With respect to the mechanism for SUA-mediated pathophysiology of NAFLD, UA has been reported to induce hepatic steatosis by stimulating fat acid synthesis, which precipitates the generation of mitochondrial oxidative stress, endoplasmic reticulum stress and SREBP-1c excessive activation (Choi et al., 2014; Lanaspa et al., 2012b). The gene discussed is SREBF1; the disease is Hepatic steatosis.