Besides the genetic polymorphism of PNPLA3 and TM6SF2, which leads to a reduction in VLDL secretion from hepatocytes and consequently to an increase in cellular TG concentration and lipid droplet content, in some cases, impairment of carbohydrate homeostasis related to incretins or alteration of pancreatic β-cell function is recognized as the primary cause for the development of MASLD, while in some individuals adipose tissue dysfunction, particularly visceral adipose tissue (VAT), has been identified [12]. This evidence concerns the gene GCG and metabolic dysfunction-associated steatotic liver disease.