FEACR directly binds to nicotinamide phosphoribosyl transferase (NAMPT) to enhance its stability and promotes the expression of NAMPT-dependent SIRT1.795 FEACR overexpression inhibits I/R-induced ferroptosis and myocardial infarction through SIRT1-forkhead box O1 (FOXO1)-FTH1 pathway, improving cardiac function.795 Therefore, FEACR and its downstream factors may be new targets for reducing ferroptosis in ischemic heart disease. The gene discussed is FOXO1; the disease is myocardial infarction.