NAFLD may result from “multiple and parallel hits” like lipotoxicity caused by the excessively elevated uptake of fatty acid (FA) into hepatocytes, subsequently elevated oxidative stress, and the activation of proinflammatory mediators of Kupffer cells (KC), as well as fibrogenic pathways of activated hepatic stellar cells (HSC), leading to non-alcoholic steatohepatitis (NASH) and non-alcoholic steatofibrosis (NASF) [5]. The gene discussed is CALCA; the disease is metabolic dysfunction-associated steatohepatitis.