To investigate the role of KLF4 in NAFLD pathogenesis, we induced steatosis in vitro by treating HepG2 cells with free fatty acid (FFA)‐bovine serum albumin (BSA) complex (palmitic/oleic acid, 1:2 ratio), or BSA as control, for 24 hours KLF4 expression was notably decreased in FFA‐treated cells as compared with BSA‐treated cells (Figure 6A), and KLF4 levels were inversely correlated with those of USP11 in FFA‐treated HepG2 cells (Figure 6B). The gene discussed is KLF4; the disease is steatosis.