Hyperactivation of the PI3K/AKT/mTOR pathway occurs in approximately 35–50% of TNBC cases, primarily driven by activating mutations in PIK3CA (15–25%) and AKT1 (5–10%), or the loss of PTEN (30–50%), leading to tumor aggressiveness and therapeutic resistance [4,5]. Here, PIK3CA is linked to neoplasm.