Focusing on the pathophysiological linkage of hypothyroidism and MAFLD, knowing the capacity of THs to modulate lipid metabolism, hypothyroidism-induced NAFLD has commonly been imputed to decreased TH activity in the liver due to reduced TH blood levels, with a consequent decrease in lipid export and utilization, and a subsequent accumulation of fat in the liver [99]. This evidence concerns the gene TH and metabolic dysfunction-associated steatotic liver disease.