It is commonly accepted that trastuzumab’s anti-tumor effects primarily function through its binding to the extracellular domain (ECD) IV of HER2, thus blocking ligand-independent HER2 dimerization and inducing antibody-dependent cell-mediated cytotoxicity (ADCC) [29,30] (Figure 1A) Other proposed mechanisms of action comprise the suppression of downstream oncogenic pathways, activation of the immune system, induction of cell cycle arrest and apoptosis, and inhibition of DNA repair [31,32,33]. This evidence concerns the gene ERBB2 and neoplasm.