Non-alcoholic fatty liver disease (NAFLD) is thought to emerge from a state of insulin resistance (IR) as the product of an interaction between the obesogenic environment and genetically predisposing alleles (e.g., I148M in PNPLA3, E167K in TM6SF2, MBOAT7 rs641738 variant) [37,38,39]. This evidence concerns the gene TM6SF2 and metabolic dysfunction-associated steatotic liver disease.