When we knocked out p53, the effect of curcumol contributing to the onset of ferroptosis was rescued, while curcumol's role in inhibiting angiogenesis was saved, which was the same effect as when we used Ferrostatin-1.<h4>Conclusions</h4>Curcumol targets the P53-TFR1-FTH1 signalling axis and induces massive deposition of iron ions in hepatic sinusoidal endothelial cells, leading to the onset of ferroptosis inhibiting hepatic angiogenesis, which may be one of the molecular mechanisms of its anti-hepatic fibrosis. The gene discussed is TP53; the disease is Hepatic fibrosis.