AMPK increases the sensitivity of human pancreatic cancer cells to cuproptosis, owing to AMPK‐induced suppression of glycolysis.[58] Similarly, ACOD1 enhances the susceptibility of CRC cells to cuproptosis by inhibiting aerobic glycolysis.[59] Our findings revealed that the AKT1 inhibitor, MK2206, inhibited glycolysis in TNBC cells, thus, the combination of elesclomol with the AKT1 inhibitor has been shown to synergistically reduce cell viability. This evidence concerns the gene AKT1 and familial pancreatic carcinoma.