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profsimonfisher.bsky.social
Simon Fisher
@profsimonfisher.bsky.social
3.4K followers 240 following 370 posts
Director of Language & Genetics at Max Planck Institute, Nijmegen.
Tracing the complex connections between genes, brains, speech & language.
Website: https://www.mpi.nl/people/fisher-simon-e
ORCID: https://orcid.org/0000-0002-3132-1996
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profsimonfisher.bsky.social
Our 3 facets: vocal production learning = ability to modify vocalizations based on experience; language structure = systematic ways in which linguistic elements relate to one another; & social underpinnings = behaviours/processes that facilitate social interaction & enable cultural transmission.10/n
Schematic to illustrate an empirical framework for the study of language evolution. The framework is both multifaceted and explicitly biocultural and is grounded in empirical investigations spanning a diverse array of fields and benefiting from major advances in methods, analyses, and theory. The potential of this integrated framework is demonstrated through three example case studies, each focused on a different facet with its own distinctive evolutionary history: vocal production learning, linguistic structure, and social underpinnings. Other facets relevant to language could be similarly investigated under this framework; such facets are represented by empty gray boxes in the schematic. Drawing on data from multiple disciplines and several species, including humans, primates, and songbirds, the case studies highlight the importance of both biological preparedness and cultural processes, as well as the interactions between them, in the emergence of language. Reproduction of the summary figure from "What enables human language? A biocultural framework" by Inbal Arnon and colleagues, published in Science (volume 390, article eadq8303).
November 23, 2025 at 12:05 PM
profsimonfisher.bsky.social
Interacting processes operating on vastly different timescales (from milliseconds to millennia) shape emergence & properties of human language(s). Roles of biology & culture, & the complex interplay between them, can be empirically investigated in humans, nonhuman animals & computational models. 8/n
Processes of language use operate at the shortest timescale, as individuals comprehend and produce utterances in ongoing conversation. Learning to form these utterances (learning sounds, words, and rules) happens over a lifetime of exposure to the language of the community. Zooming out further, the structure of a specific language emerges and changes through cultural evolution, as knowledge of language is passed from one generation to the next. Lastly, the cognitive and anatomical machinery that allows humans to learn and use language has been subject to genetic evolution over the course of human evolution. The processes of biological and cultural evolution interact to produce a dual-inheritance system. Features of languages are inherited culturally, and the mechanisms that support such cultural inheritance are themselves inherited genetically. These processes may interact in complex and interesting ways, studied using mathematical and computational models that include all three timescales: individual learning and use, cultural evolution, and biological evolution. Reproduction of Figure 1A from "What enables human language? A biocultural framework" by Inbal Arnon and colleagues, published in Science (volume 390, article eadq8303).
November 23, 2025 at 11:54 AM
profsimonfisher.bsky.social
Unboxing Schrödinger's cat.
Opening a shoebox reveals the contents: a beautiful (and very much alive) tortoise-shell cat, with an orange streak on its forehead.
November 3, 2025 at 9:57 PM
profsimonfisher.bsky.social
For a deeper dive into what's known about neural functions of FOXP2 & its interactors, see our review on “Molecular networks of the FOXP2 transcription factor in the brain” by Joery den Hoed et al, which also framed key questions for future investigation:
www.embopress.org/doi/full/10....
🗣️🧠🔬🧬 12/12
Schematic to illustrate different levels of FOXP2 functioning, organized in panels from left to right, to highlight questions that should be focus of future studies. First (leftmost) panel shows a silhouette of a person speaking, with the following questions below: "Why do FOXP2 variants have disproportionate effects on speech and language skills in humans, as compared to other cognitive functions? What explains similarities and differences between phenotypes associated with FOXP1, FOXP2 and FOXP4 dysfunction?" Second panel shows a cross-section of a human brain with shaded brain areas representing regions of expression of FOXP2 that have been main focus in current literature. The question below is: "How, and at which stages, is FOXP2 crucial in brain development?" Third panel shows a schematic of different types of neuronal progenitors and neurons. The question below is: "Which aspects of cell differentiation and function are dependent on FOXP2?" Fourth panel shows a schematic of a single cell with a nucleus and cytoplasm, and molecules moving/interacting within them. The question below this is: "And which molecular pathways are mediated by FOXP2?" Final (rightmost) panel shows a schematic of the FOXP2 protein undergoing post‐translational modifications (labelled as PTMs), binding to protein interactors (labelled as int), including other transcription factors (labeled as TFs), and interacting with DNA, shown as a double-helix. The questions below are: "How is FOXP2 expression and function modulated at the molecular level in diverse tissues and at different developmental time points? How does FOXP2 control chromatin remodeling and target gene expression? Can newly available tools help to dissect out downstream pathways?" The image comes from Figure 3 of a paper entitled “Molecular networks of the FOXP2 transcription factor in the brain” written by den Hoed, Devaraju and Fisher, and published in the journal EMBO Reports in August 2021 (Volume 22, article e58203).
October 31, 2025 at 6:03 PM
profsimonfisher.bsky.social
The story began with a three-generation family in which 15 relatives had speech & language impairments. We found that all affected (but no unaffected) family members had inherited the same unusual FOXP2 variant, one that altered a key part of the encoded protein, interfering with its functions. 2/n
Image shows a pedigree diagram (family tree) across three successive generations. As is standard for these types of diagrams, it uses squares to indicate males and circles to indicate females, with generations arranged from top to bottom. 15 of the family members are shaded in black which is used to show that they are affected with a developmental speech & language disorder, while the remaining relatives are unaffected. The pattern of inheritance (about half members of each generation affected, males and females in similar number) appears consistent with a classic monogenic (single-gene) dominant mode of transmission, of the kind you might see in a human genetics textbook. Studies of this family led to the discovery of the FOXP2 gene in 2001.
October 29, 2025 at 5:09 PM
profsimonfisher.bsky.social
More than two decades have passed since we discovered that rare disruptions of the FOXP2 gene disturb development of proficient speech/language skills. Today we know of multiple FOXP genes that are directly implicated in distinct brain-related conditions with differences in symptoms & severity.🧪 1/n
A depiction of expression patterns of the FOXP1, FOXP2, and FOXP4 genes in the brain, based on the developmental human RNA sequencing dataset of BrainSpan (http://www.brainspan.org/). Data cover different prenatal timepoints starting at 8-to-10 weeks postconception (abbreviated as pcs), postnatal timepoints from 0-to-12 months (abbreviated as mos), and expression measured in adulthood. A dashed vertical line represents time of birth. Individual dots are shown each representing one brain sample, and lines show loess curves fitted through the datapoints. The analyzed brain regions are A1C, primary auditory cortex; CB, cerebellum; CBC, cerebellar cortex; DFC, dorsolateral prefrontal cortex; DTH, dorsal thalamic nucleus; HIP, hippocampus; IPC, inferior parietal cortex; ITC, inferior temporal cortex; M1C, primary motor cortex; MD, mediodorsal thalamic nucleus; MFC, medial frontal cortex; OFC, orbitofrontal; S1C, primary sensory cortex; STR, striatum; TC, superior temporal cortex; V1C, primary visual cortex; VFC, ventromedial prefrontal cortex. This image comes from Figure 1 of a paper entitled “Molecular networks of the FOXP2 transcription factor in the brain” written by den Hoed, Devaraju and Fisher, published in the journal EMBO Reports in August 2021 (Volume 22, article e58203).
October 29, 2025 at 5:09 PM
profsimonfisher.bsky.social
Come join us for a 4-year PhD on effects of rare gene disruptions involved in speech disorder, investigated in human neuronal models (via gene-editing, tissue culture, brain organoids, high-res microscopy, transcriptomics, epigenomics).
More info: www.mpi.nl/imprs-phd-fe...
#AcademicJobs #PhDJobs
🧬🧪
Photograph of researchers at their benches in the custom-built molecular biology labs of the Max Planck Institute in Nijmegen, with green trees of the forest outside visible through large windows in the background.
October 22, 2025 at 3:43 PM
profsimonfisher.bsky.social
Help spread the word about developmental language disorder, a common yet often hidden condition that makes it hard for children to understand what's said to them & to articulate thoughts & feelings. Lots of helpful resources & information at radld.org.
#DLDday #DevLangDis @radld.bsky.social
Flyer on Developmental Language Disorder, prepared by the organisation RADLD (Raising Awareness of Developmental Language Disorder). The flyer has the title "You can't see DLD" and shows a photograph of a boy in a blue short-sleeved shirt and khaki trousers, against a purple background. To the right of him there are lines of text which read: - Started to talk later than his siblings - Has difficulties learning new words - Needs lots of repetitions to follow instructions - Struggles to join activities & discussions The bottom of the flyer says "Support #DLDday on Friday 17th October 2025. Learn more at RADLD.ORG".
October 17, 2025 at 9:34 AM
profsimonfisher.bsky.social
In the years that followed, rare FOXP2 disruptions have been found in multiple other families with problems in speech, language & behaviour, refining understanding of the associated disorder, while the impacts of its dysfunction have been studied in detail in animal models & cellular systems. 17/n
Schematic image showing diverse approaches that have been used for studying the roles of the FOXP2 gene in the brain over past couple of decades. The lefthand panel shows a pedigree diagram of the three-generation KE family, investigations of whom led to discovery of the first FOXP2 mutation. The middle panel shows molecular functions of FOXP2, how it interacts with multiple other proteins and regulates chromatin condensation and aspects of neuronal maturation. The righthand panel shows its effects on neurobiological pathways and behaviour as identified in animal models such as mice and songbirds, with a focus on the cortex, striatum and cerebellum of the brain. Figure 1 from the paper “Genetic pathways involved in human speech disorders” by Joery den Hoed and Simon Fisher, published in Current Opinion in Genetics and Development in 2020 (volume 65, pages 103 to 111).
October 4, 2025 at 5:18 PM
profsimonfisher.bsky.social
Based on its DNA-binding motif, this was a novel FOX transcription factor, & it was given the official name FOXP2. Prior literature had linked pathogenic variants in other FOX genes to a range of diseases. Our work suggested FOXP2 dysfunction as one potential cause of speech/language disorder. 16/n
Amino-acid sequences of the forkhead domains of three FOXPs, aligned with representative proteins from several branches of FOX transcription factor proteins. All sequences are from Homo sapiens. Residues that are invariant in this selection of forkhead proteins are given beneath the alignment. Asterisks show sites of the substitution mutations in FOXC1, FOXE1 and FOXP3 that had been previously implicated in human disease states. The upwards arrow indicates the site of the R553H substitution identified in FOXP2 in affected members of the KE pedigree. The proposed structure of the forkhead domain as established by X-ray crystallography is shown, containing three α-helices, three β-strands, and two ‘wings’. Figure 4 from the paper “A forkhead-domain gene is mutated in a severe speech and language disorder” by Cecilia Lai and colleagues, published in Nature in 2001 (volume 413, pages 519-523).
October 4, 2025 at 3:14 PM
profsimonfisher.bsky.social
When we sequenced this newly discovered section of the gene in the KE family, we found a single nucleotide variant (guanine-to-adenine) in all the affected members, yielding an amino-acid change (arginine-to-histidine) at a critical place in the FOX domain, predicted to disrupt its function. 15/n
Image shows example Sanger DNA sequencing traces for one part of FOXP2 in unaffected (top) and affected (bottom) members of the KE family. The sequencing uncovered a guanine-to-adenine (G-to-A) transition that leads to an R553H substitution in the forkhead domain of the encoded protein in the affected individuals. All affected individuals from the KE pedigree are heterozygous for this variant, whereas all unaffected individuals are homozygous for the reference version. Adapted from Figure 3 in the paper “A forkhead-domain gene is mutated in a severe speech and language disorder” by Cecilia Lai and colleagues, published in Nature in 2001 (volume 413, pages 519-523).
October 4, 2025 at 2:28 PM
profsimonfisher.bsky.social
Then, another twist! Turned out that CAGH44 was mischaracterized by the team who had originally cloned it. Our data showed that the gene extends much further than they had thought. Reconstructing the entire locus, we found a key part encoding a forkhead box (FOX), a type of DNA-binding domain. 14/n
Representation of the basic human FOXP2 gene structure on chromosome 7. Boxes represent exons, with positions of initiation and termination codons indicated. The scale shown applies only to exons; the entire region depicted spans more than 267 kb of genomic DNA. Exons encoding polyglutamine tracts (PolyQ) and the forkhead domain (FOX) are indicated. The previously known CAGH44 transcript only covered exons 2–7, missing a large part of the gene. Bacterial artificial chromosome genomic sequence entries are aligned beneath the gene structure. Part of Figure 2 in the paper “A forkhead-domain gene is mutated in a severe speech and language disorder” by Cecilia Lai and colleagues, published in Nature in 2001 (volume 413, pages 519-523).
October 4, 2025 at 2:17 PM
profsimonfisher.bsky.social
This unrelated child had a translocation involving exchange of material between chromosomes 7 & 5. We mapped the chromosome 7 breakpoint to our region of interest, very close to CAGH44, a brain-expressed polyglutamine-tract gene. But alas we did not find any changes in CAGH44 in the KE family. 13/n
Microscope images showing the chromosomes of a child who carried a genomic rearrangement - a translocation involving chromosomes 7 and 5. The child was unrelated to the KE family but showed a very similar speech and language disorder to them. The locations of the chromosomal breakpoints are visualized here using a special cytogenetics technique known as metaphase fluorescence in-situ hybridization. Part of Figure 4 in the paper “The SPCH1 region on human 7q31: genomic characterization of the critical interval and localization of translocations associated with speech and language disorder” by Cecilia Lai and colleagues, published in the American Journal of Human Genetics in 2000 (volume 67, pages 357 to 368)
October 4, 2025 at 2:07 PM
profsimonfisher.bsky.social
Our genomic region of interest was big, only partially characterized & likely to include many unknown genes. It was 1998, some years before the Human Genome Project finished a first draft. As sections of sequence became available, I used bioinformatic approaches to build maps of the interval. 11/n
Image shows a bioinformatic map aligning contiguous sections of sequence data corresponding to one part of chromosome 7, with respect to a set of known genetic markers. One of the bottom rows shows individual protein-coding genes that were predicted by analysing the DNA sequence information. Taken from Figure 2 of the paper “The SPCH1 region on human 7q31: genomic characterization of the critical interval and localization of translocations associated with speech and language disorder” by Cecilia Lai and colleagues, published in the American Journal of Human Genetics in 2000 (volume 67, pages 357 to 368)
October 4, 2025 at 1:45 PM
profsimonfisher.bsky.social
But even as debates ensued on the nature of the disorder, DNA-based methods hadn’t yet been used to test if its inheritance was truly monogenic. By tracing transmission of genetic markers in the family, we confirmed involvement of a single locus, & localized it to one part of chromosome 7.
10/n
Image shows first two printed pages of “Localisation of a gene implicated in a severe speech and language disorder” by Simon Fisher and colleagues, published in Nature Genetics in 1998 (volume 18, pages 168 to 170). The abstract reads: Between 2 and 5% of children who are otherwise unimpaired have significant difficulties in acquiring expressive and/or receptive language, despite adequate intelligence and opportunity. While twin studies indicate a significant role for genetic factors in developmental disorders of speech and language, the majority of families segregating such disorders show complex patterns of inheritance, and are thus not amenable for conventional linkage analysis. A rare exception is the KE family, a large three-generation pedigree in which approximately half of the members are affected with a severe speech and language disorder which appears to be transmitted as an autosomal dominant monogenic trait. This family has been widely publicised as suffering primarily from a defect in the use of grammatical suffixation rules, thus supposedly supporting the existence of genes specific to grammar. The phenotype, however, is broader in nature, with virtually every aspect of grammar and of language affected. In addition, affected members have a severe orofacial dyspraxia, and their speech is largely incomprehensible to the naive listener. We initiated a genome-wide search for linkage in the KE family and have identified a region on chromosome 7 which co-segregates with the speech and language disorder (maximum lod score = 6.62 at theta = 0.0), confirming autosomal dominant inheritance with full penetrance. Further analysis of microsatellites from within the region enabled us to fine map the locus responsible (designated SPCH1) to a 5.6-cM interval in 7q31, thus providing an important step towards its identification. Isolation of SPCH1 may offer the first insight into the molecular genetics of the developmental process that culminates in speech and language.
October 4, 2025 at 1:34 PM
profsimonfisher.bsky.social
The London team countered the claim; in-depth work by neuroscientists Faraneh Vargha-Khadem & @kateewatkins.bsky.social showed the most profound feature of the KE family disorder is impaired sequencing of mouth/face movements underlying speech, with multiple aspects of language also affected. 9/n
The image shows Table 1 from a paper by Faraneh Vargha-Khadem and colleagues, published in the Proceedings of the National Academy of Sciences in 1995 (volume 92, pages 930 to 933). The Table displays comparisons of performance of affected and unaffected members of the KE family on a wide array of different tests of language skills, finding significant differences for almost every aspect tested.
October 4, 2025 at 1:34 PM
profsimonfisher.bsky.social
Long before anyone started studying the DNA, reports of the family fueled controversy over existence of a dubious “grammar gene”. Extensive coverage had been given to linguist Myrna Gopnik’s claim of a selective deficit in grammar skills e.g. that KEs “lack a general rule for producing plurals”. 8/n
The left-hand side of the image shows the one-page correspondence that the Canadian linguist Myrna Gopnik wrote to Nature in 1990 (volume 344, page 715) arguing that members of the KE family have a selective deficit in “the accurate usage of syntactical-semantic features of language, such as the significance of number, gender, animacy, proper names, tense and aspect” and that they “lack a general rule for producing plurals”. The right-hand side of the image shows the “wug” test, one of the tests that Gopnik refers to in her correspondence, highlighted as something that affected KE family members fail on. The top part shows a single simply-drawn imaginary animal, with the text “This is a wug” underneath. The bottom part shows two of these imaginary animals side by side, accompanied by the text “Now there is another one. There are two of them. There are two ......”. The person being tested has to respond by completing correctly the end of this statement (i.e. producing the plural “wugs”).
October 4, 2025 at 1:34 PM
profsimonfisher.bsky.social
Soon after we had begun building up cohorts for the project, Tony was contacted by Marcus Pembrey, a leading geneticist at London’s Institute of Child Health. His team had identified a 3-generation British family (codename KE) in which 15 relatives had problems with speech/language development. 6/n
Image shows a pedigree diagram (i.e. family tree) for the KE family, across three successive generations. As is standard for these types of diagrams, it uses squares to indicate males and circles to indicate females, with generations arranged from top to bottom. 15 of the family members are shaded in black, which is used to show that they are affected with a developmental speech & language disorder, while the remaining relatives are unaffected. The pattern of inheritance (about half members of each generation affected, males and females in similar number) appears consistent with a classic monogenic (single-gene) dominant mode of transmission, of the kind you might see in a human genetics textbook.
October 4, 2025 at 1:34 PM
profsimonfisher.bsky.social
Twenty-four years ago today, our paper “A forkhead-domain gene is mutated in a severe speech and language disorder” was published: www.nature.com/articles/350....
A personal thread about the ups & downs of the journey we took to get to that point....1/n
🗣️🧬🧪
Image shows the first two printed pages of the paper “A forkhead-domain gene is mutated in a severe speech and language disorder” by Cecilia Lai and colleagues, published in Nature in 2001 (volume 413, pages 519-523). The abstract reads as follows: Individuals affected with developmental disorders of speech and language have substantial difficulty acquiring expressive and/or receptive language in the absence of any profound sensory or neurological impairment and despite adequate intelligence and opportunity. Although studies of twins consistently indicate that a significant genetic component is involved, most families segregating speech and language deficits show complex patterns of inheritance, and a gene that predisposes individuals to such disorders has not been identified. We have studied a unique three-generation pedigree, KE, in which a severe speech and language disorder is transmitted as an autosomal-dominant monogenic trait. Our previous work mapped the locus responsible, SPCH1, to a 5.6-cM interval of region 7q31 on chromosome 7. We also identified an unrelated individual, CS, in whom speech and language impairment is associated with a chromosomal translocation involving the SPCH1 interval. Here we show that the gene FOXP2, which encodes a putative transcription factor containing a polyglutamine tract and a forkhead DNA-binding domain, is directly disrupted by the translocation breakpoint in CS. In addition, we identify a point mutation in affected members of the KE family that alters an invariant amino-acid residue in the forkhead domain. Our findings suggest that FOXP2 is involved in the developmental process that culminates in speech and language.
October 4, 2025 at 1:34 PM
profsimonfisher.bsky.social
Why does this matter? Sensational stories hailing a dramatic rewrite of human origins are regularly repurposed by some as a tool to undermine the legitimacy of evolution. Take this example of Mike Pence talking to US Congress way back in 2002. Full transcript: www.congress.gov/congressiona...
...4/n
Selection of the transcript from Mike Pence's speech about the "THEORY OF THE ORIGIN OF MAN" from the US Congressional Record, July 11th, 2002. Pence's speech went as follows: "It is what we have been taught, that man proceeded and evolved along linear lines. But now comes a new find by paleontologists. In the newspapers all across America, a new study in "Nature" magazine, 6- to 7-million-year-old skull has been unearthed, the Toumai skull and it suggests that human evolution was actually, according to a new theory, human evolution was taking place, and I am quoting now, "all across Africa and the Earth," and the Earth was once truly, and I quote, "a planet of the apes on which nature was experimenting with many human-like creatures." Paleontologists are excited about this, Mr. Speaker. But no one is pointing out that the textbooks will need to be changed because the old theory of evolution taught for 77 years in the classrooms of America as fact is suddenly replaced by a new theory, or I hasten to add, I am sure we will be told a new fact. The truth is it always was a theory, Mr. Speaker. And now that we have recognized evolution as a theory, I would simply and humbly ask, can we teach it as such and can we also consider teaching other theories of the origin of species? Like the theory that was believed in by every signer of the Declaration of Independence...."
September 27, 2025 at 1:43 PM
profsimonfisher.bsky.social
New analysis of a 1-million yr old fossil skull captured worldwide media attention this week, with many headlines saying it requires a complete rewrite/rethink of human evolution. This is an intriguing study & it's brilliant to see so much public enthusiasm for deciphering our origins, but....1/n 🧪
Image shows just two example headlines from prominent media outlets earlier this week, heralding a newly published discovery that supposedly "rewrites human evolution". Left side, from the BBC: "Million-year-old skull rewrites human evolution, scientists claim"; right side, from the New York Post: "1M-year-old skull discovery could change everything we know about human evolution".
September 27, 2025 at 12:40 PM
profsimonfisher.bsky.social
This goes to eleven.
A cartoon by Tom Gauld about what happens when you turn it up to eleven. Two scientists are in front of a computer terminal, observing the screen. The first scientist explains: "The simulator can replicate our world at various levels of detail. Level one presents you as a rudimentary icon." The second scientist looks at the screen which indeed shows a very low resolution image of his head. The first scientist goes on: "Whereas level ten is almost identical to the real you." The image now showing on the screen looks just like the second scientist (i.e. a Tom Gauld styled cartoon depiction of his head). The second scientist is impressed. "Incredible! What happens at level eleven?", he asks. Ignoring the first scientist's warning ("Don't press that!"), he rashly pushes a big button labelled "11" which gives a satisfying click. "Aaagh!" cries the shocked man. The screen now shows a dramatically more realistic image of him than anywhere in the rest of the cartoon.
September 6, 2025 at 4:24 PM
profsimonfisher.bsky.social
Applications open for fully funded 4-yr positions in the unique interdisciplinary program of the @maxplanck.de School of Cognition. Pursue a passion for science at the forefront of fundamental & applied research, mentored by a network of world renowned researchers.🧪
cognition.maxplanckschools.org/en
Flyer advertising the Max Planck School of Cognition 4-year PhD fellowship programme, with a photograph of prior fellows. Interdisciplinary research, outstanding faculty, fully financed. You can now apply, sign up for the Applicant Support Program, and/or register for a Q & A session, all via the webpage: cognition.maxplanckschools.org
September 4, 2025 at 12:08 PM
profsimonfisher.bsky.social
A reminder that there is no scientific basis for attempts to define people in terms of “good” or “bad” genes - these are discredited views in service of racist ideologies. For the consensus from the experts, see e.g. this 2020 @geneticssociety.bsky.social statement:
www.ashg.org/publications... 🧬🧪
Statement from the American Society of Human Genetics in 2020, countering the myth of "good genes". It reads as follows: "Genetics demonstrates that humans cannot be divided into biologically distinct subcategories or races, and any efforts to claim the superiority of humans based on any genetic ancestry have no scientific evidence. Moreover, it is inaccurate to claim genetics as the determinative factor in human strengths or outcomes when education, environment, wealth, and health care access are often more potent factors. There is no factual basis for attempts to define communities or regions of people with "good" or "bad" genes and a century of science has debunked such claims, which can feed discredited views and racist ideologies. Unchecked, unethical application of false genetic "theories" have resulted in past atrocities from forced sterilizations to the Holocaust and can still fuel unethical social policies worldwide today. Over the decades, our field also has reflected on its own role in such now-condemned ideas, and we speak out vocally as a community and as individuals to combat their resurgence. We must protect and advance the ethical use of genetics and genomics knowledge for the profound good it can realize, including better, more precise healthcare that leverages what we are discovering about human genetic commonality and diversity. The human genetics community dedicates itself to this goal each day, and today we are improving and saving hundreds of thousands of lives. As the ASHG community focuses on realizing the benefits of human genetics and genomics research for people everywhere, we also urge societal attention to address profound educational, economic and health inequalities that fuel differences in human experience and well-being. By pursuing all of these activities, humans can celebrate our common heritage as one people, embrace and fully tap our valued diversity, and help achieve optimal life outcomes for all."
August 29, 2025 at 5:48 PM
profsimonfisher.bsky.social
Saw this today and smiled.
Correlation or causation?
Classic xkcd webcomic by Randall Munroe, depicting a brief discussion between two people. Person A: I used to think correlation implied causation. Then I took a statistics class. Now I don't. Person B: Sounds like the class helped. Person A: Well, maybe.
August 22, 2025 at 3:11 PM