This might be explained by, 1) although FGF15 protein was very high in liver, it was unable to suppress hepatic CYP7A1 expression 33 for BA synthesis and BAs could induce liver injury and cell death 46; 2) the BAs mediated up-regulation of FGFR4 in hepatocytes 48 could not only promote hepatic lipid accumulation 24, 36 but also induce regeneration 47, causing repetitive injury/repair in liver; and 3) lack of FGF21 further worsened steatosis and the NASH progression. The gene discussed is FGF21; the disease is steatosis.