That is, ferroptosis can not only function as the liver fibrosis and HCC therapeutic strategy, but can also induce many other liver diseases, such as NAFLD, ALD, NASH, IRI, etc. As shown in Figure 1, the common mechanisms of ferroptosis include GPX4 inhibition, FSP1 suppression, GCH-1 restraint, system Xc− suppression, lipid peroxide accumulation and iron overload. This evidence concerns the gene GCH1 and metabolic dysfunction-associated steatohepatitis.