Studies have shown that deficiency of liver ATGL causes hepatic steatosis but not NASH or fibrosis,17 whereas hepatic CGI-58 deficient mice exhibit pronounced hepatic steatosis and later develop NASH and liver fibrosis, accompanied by increases in TNFα and α-SMA.18 Individuals with CGI-58 loss-of-function mutations typically experience severe hepatic steatosis, NASH, and cirrhosis.19 Our results showed that KAL up-regulated the expression and secretion of TNFα in primary hepatocytes (Fig. 4j-l), which could be inhibited by CGI-58 but not ATGL (Fig. 4m–o). This evidence concerns the gene ACTA1 and fatty liver disease.