In consistent with this outcome, Liu et al. have illuminated that the degradation of NEAT1 had the capacity to reduce the levels of diacylglycerol and free fatty acid in rat HCC models, thereby modulating the abnormal lipid metabolism in hepatocytes [26], and Zadjali et al. have pointed out that the inhibition of SOCS2 could protect against hepatic steatosis in mice that fed with high-fat-diet [20]. The gene discussed is SOCS2; the disease is Hepatic steatosis.