To develop successful targeted therapies, many investigations have focused on the phosphoinositide 3-kinase (PI3K) pathway, whose altered genetic activation is reported in 25–35% of TNBC and contributes to tumor growth, metastasis, and drug resistance.1, , , , –6 The essential components of the pathway include PI3Ks, Akt serine/threonine kinase family (AKT), mammalian target of rapamycin (mTOR), and phosphatase and tensin homolog (PTEN). This evidence concerns the gene MTOR and neoplasm.