Consistent with this protective role, we found that mice lacking Fth in cardiomyocytes develop ferroptosis-induced cardiomyopathy.24 Notably, ferritinophagy—an NCOA4 (nuclear receptor coactivator 4)-mediated autophagic degradation of ferritin in the lysosome—has been shown to induce ferroptosis by releasing free iron from ferritin.26,27 Moreover, the iron exporter ferroportin (FPN) has also been shown to regulate cellular sensitivity to ferroptosis in vitro.28 The gene discussed is SLC40A1; the disease is cardiomyopathy.