Furthermore, Imajo et al. reported that increased levels of leptin lead to overexpression of CD14 via activation of STAT3 signaling in Kupffer cells, resulting in a hepatic hyperinflammatory response to gut-derived low-dose bacterial endotoxin and progression from simple steatosis to steatohepatitis with associated liver inflammation and fibrosis [77]. The gene discussed is STAT3; the disease is steatosis.