In the glucocorticoid (GC)-induced NAFLD model, trans-activated FTO induced hepatocyte adipogenesis and lipid accumulation by mediating the demethylation of sterol regulatory element binding factor 1 (SREBF1) and SCD1 [124], while FTO promoted the progression of chronic liver inflammation by mediating demethylation of interleukin-17 (IL-17) [125], indicating the critical role of FTO in the development of NAFL and NASH to HCC. The gene discussed is FTO; the disease is metabolic dysfunction-associated steatotic liver disease.