Among the former, the following may be included: (1) ERBB2 truncation, (2) impaired binding of Tz to HER2, (3) activation of compensatory or alternative signaling pathways, (4) defects in apoptosis and cell cycle control, (5) increased ability to generate cancer stem cells, (6) vascular mimicry and hypoxia, and (7) metabolic adaptation. This evidence concerns the gene ERBB2 and cancer.