Dysregulation of this pathway, commonly observed in TNBC, contributes to enhanced cancer cell survival, growth, and chemotherapy resistance.[34] The three isoforms of Akt (Akt1, Akt2, and Akt3) are encoded by distinct genes, exhibit high sequence similarity, and are activated through near‐identical mechanisms.[35] However, they demonstrate different or even opposing functions in regulation of TNBC development.[36, 37] Previous studies confirmed that targeting the AKT pathway could be an effective therapeutic strategy for TNBC. This evidence concerns the gene AKT1 and cancer.