Studies revealed a number of molecular mechanisms associated with the trastuzumab resistance [7,8], including (i) HER2 mutation defective in binding with trastuzumab (i.e., HER2 truncation), (ii) upregulation of HER2 downstream signalings (i.e., PTEN loss), (iii) activation of alternative signaling pathways (i.e., IGF1R stimulation), and (iv) failure to trigger antibody-mediated anti-cancer immunity (i.e., FcγRIII F158 polymorphism). This evidence concerns the gene ERBB2 and cancer.