HER-2 overexpression is considered an oncogenic driver that promotes constitutive activation of downstream signaling cascades related to cell survival/proliferation through MAPK pathway (Ras mitogen–activated protein kinase) or inhibition of cell death through PI3K/Akt/mTOR pathway [6]; trastuzumab resistance is associated with downstream signal activation, tumor stem cell self-renewal, host immune regulation, and epigenetic effects. This evidence concerns the gene ERBB2 and neoplasm.