IRP2 is primarily regulated by iron‐mediated degradation, and IRP1 responds to iron‐dependent and iron‐independent signals that control its function through multiple mechanisms to maintain suitable IRE‐binding activity for cellular iron homeostasis.[28, 29] Notably, although IRP1 is not differentially expressed between tumor and normal tissues in ESCC, it is still able to promote cell proliferation, and upregulation of IRP1 predicts unfavorable outcomes in patients with ESCC, implying a possible oncogenic role of IRP1. Here, IREB2 is linked to neoplasm.