While the previous studies that breast cancer patients resistant to endocrine therapy exhibiting stronger PI3K inhibitor treatment sensitivity had frequent occurrence of PI3K mutations and overactivation of the PI3K/Akt/mTOR signaling36 suggested the need for future focus on the characterization of the molecular and genomic signatures to identify lymphoma patients who could better benefit from TQ-B3525. This evidence concerns the gene AKT1 and breast cancer.