For years, the “two-hit” theory was the prevailing one; according to this theory, the pathophysiology of NAFLD consisted of a first “hit” representing the stage of simple steatosis with lipid accumulation and insulin resistance [20], followed by a second “hit”, leading to oxidative and endoplasmic reticulum (ER) stress, leading to the development and progression of hepatic inflammation and fibrosis. The gene discussed is INS; the disease is metabolic dysfunction-associated steatotic liver disease.