Meanwhile, the liver-specific ablation of MFN2 in mice has been reported to induce inflammation, fibrosis, and even liver cancer, whereas the overexpression of MFN2 was able to ameliorate CCl4-induced liver fibrosis by inhibiting the TGF-β1/Smad signaling pathway and downregulating collagen levels, such as type I, type III, and type IV collagen [52,53]. The gene discussed is TGFB1; the disease is Hepatic fibrosis.