Per sort jo tinc un pla infalible

And because Bsky doesn't seem very fond of image transparencies, here is a version of the image with a white background:

All the above analyses were run in UK Biobank. But we found that the interaction effects could be replicated in the All of Us Research Program Cohort.

We also found evidence of amplification of the effect of risk alleles at the BCAR1, SMARCA4, TGF-β, and EDNRA loci. Interestingly, the flux amplifying the effect of variants mapped to the TGF-β loci involved a reaction with a key role in glycosylation and the activation of purinergic receptors.

Many of the interactions reflected potentially interesting biology. For instance, increased capacity to transport prostaglandin, a known inflammatory mediator, amplified the effect of CAD risk alleles while diverting arachidonic acid away from prostaglandin synthesis had a buffering effect.

Our analysis identifies 30 risk locus - reaction flux pairs with significant interaction on CAD susceptibility. For instance, we found many significant interactions between reaction fluxes and risk alleles mapped to four risk loci in the chromosome 6 genomic region encoding the LPA and PLG genes.

In this work, we use genetically predicted reaction fluxes to perform a systematic search for metabolic fluxes acting as buffers (negative interaction effect) or amplifiers (positive interaction effect) of coronary artery disease (CAD) risk alleles in UK Biobank.