GWAS found consistent associations between gene variants, such as TM6SF2, and NAFLD, offering new insights and potential drug targets.[45] This suggests that metabolic changes related to diabetes override the effects of the TM6SF2 variant in the early stages of diabetes and NAFLD.[46] Hepatic IR is a key mechanism when considering FLD as a T2DM risk factor. This evidence concerns the gene TM6SF2 and metabolic dysfunction-associated steatotic liver disease.