Our previous study revealed that AKT1 phosphorylated SIK1, thereby disrupting its tumor‐suppressive function.[52] Moreover, AKT1 is also closely associated with tumor tolerance to cell death.[53] AKT1 directly phosphorylates key apoptotic regulators such as BAD, Caspase‐9, and BIM, thereby inhibiting tumor apoptosis.[54] In addition, AKT1 directly phosphorylates TRPML1 at Ser343, and prevents its degradation of TRPML1, which leads to ferroptosis inhibition.[55] In this study, we found that AKT1 inhibited cuproptosis in TNBC by phosphorylating FDX1. The gene discussed is BAD; the disease is neoplasm.