While current therapies (endocrine therapy, targeted agents, etc.)have improved patient outcomes [4,5,6,7], critical challenges persist: the rapid development of drug resistance (e.g., ER signaling reactivation via ERα mutations or PI3K/AKT pathway activation in tamoxifen resistance [8,9], acquired resistance to HER2-targeted therapies [8]), tumor spatiotemporal heterogeneity (molecular subtype variations [9], clonal evolutionary diversity [10]), and treatment-related toxicities (anthracycline-induced cardiotoxicity [11], immune checkpoint inhibitor-related autoimmunity [12]). Here, AKT1 is linked to neoplasm.