In addition, we confirmed that Fe (II) was significantly reduced when the NPC1−/− HEI-OC1 cells were treated with wortmannin or chloroquine (Figure 3C), suggesting that inhibiting autophagy by either repressing autophagosome synthesis or blocking autophagosome degradation could relieve the NPC1 deficiency–induced iron metabolic disorders. This evidence concerns the gene NPC1 and iron metabolism disease.