Further, both ALD and NAFLD share a genetic predisposition that contributes to their disease progression through hepatic fat accumulation (PNPLA3, TM6SF2, GCKR, GPAM, APOB, PYGO1, etc.), oxidative and ER stress (HFE, MARC1, SOD2, UCP2, SERPINA1), inflammation and fibrogenesis (PNPLA3, HDS17B13, MERTK, LEPR) [52]. This evidence concerns the gene PNPLA3 and metabolic dysfunction-associated steatotic liver disease.