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]. This evidence concerns the gene CD14 and steatosis.