NCOA4 and cancer: Furthermore, excessive copper regulated the autophagy flux by directly modulating the expression of ATG proteins, such as ATG‐5, Beclin1, p62, and MAP1LC3.[52] The oxidative stress caused by copper could also promote autophagy through activating the AMP‐Activated Protein Kinase (AMPK)‐ Mammalian Target of Rapamycin (mTOR) pathway.[53] Despite the lack of evidence for the direct interaction between copper and NCOA4, it is conceivable that exploiting the regulatory characteristics of copper on autophagy might be an effective strategy for potentiating ferroptosis to benefit cancer treatment.