HER2 overexpression serves as an oncogenic driver in the progression of BC, promoting constitutive activation of downstream signaling cascades that induce cell proliferation through the Ras-mitogen-activated protein kinase (MAPK) pathway, or inhibit cell death through the phosphatidylinositol 3′-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway [6, 7]. This evidence concerns the gene MTOR and breast cancer.