To date, GWAS have identified numerous variants that pose a risk for MASLD; although these variants influence a number of metabolic processes such as intestinal lipid absorption, insulin sensitivity, hepatic lipogenesis and mitochondrial respiration (9, 10), the two variants with the highest significance in nearly all GWAS — PNPLA3 (patatin-like phospholipase domain-containing protein 3) and TM6SF2 — both affect hepatic lipid disposal (16, 17). Here, INS is linked to metabolic dysfunction-associated steatotic liver disease.