This paradox can be partially explained by the identification of somatic mutations in genes involved in the regulation of lipid metabolism (forkhead transcription factor O1, FOXO1; cell-death-inducing DFFA-like effector b, CIDEB; and glycerol-3-phosphate acyltransferase, GPAM) in patients with advanced NAFLD [35]. The gene discussed is CIDEB; the disease is metabolic dysfunction-associated steatotic liver disease.