The key protein of cuproptosis, DLAT, was discovered to potentially promote tumorigenesis of diverse cancers by stimulating autophagy, thereby endowing it with the function of an oncogene.[178] However, in the cuproptosis of prostate cancer induced by elesclomol‐Cu, the lipoylation of DLAT inhibited autophagy by activating mTOR, which sensitized cells to docetaxel.[179] This indicates that there might be differences in the regulation of autophagy by DLAT in the normal state and the cuproptosis state. This evidence concerns the gene DLAT and cancer.