Moreover, reduced Mfn2 levels are observed in the liver biopsies from patients with NASH and in the mouse models of steatosis and NASH; Mfn2 re-expression ameliorates the disease in the NASH model mice, whereas, liver-specific deletion of Mfn2 induces inflammation, triglyceride accumulation, fibrosis, and liver cancer [143]. This evidence concerns the gene MFN2 and steatosis.