MYCBP2 inhibits signaling pathways that drive hepatic steatosis, including mTOR and p38 MAPK [36–39], while also suppressing adipogenesis by promoting SMAD4 ubiquitination [40], possibly explaining why aggregated deleterious variants in MYCBP2 were positively associated with both MASLD and body fat percentage. This evidence concerns the gene SMAD4 and fatty liver disease.