ERBB2 and cancer: The latter can be summarized as follows: (i) impaired binding of Tz to HER2, due to expression of receptor variants [15] or molecular masking [16]; (ii) interaction of HER2 with other dimerization partners, such as HER-family receptors [17] or insulin-like growth factor-1 receptors 1 and 2 (IGFR 1/2) [18]; (iii) constitutive activation of the PI3K/AKT/mTOR axis [19]; (iv) activation of alternative signaling pathways [20]; (v) increased ability to generate cancer stem cells [21]; (vi) vascular mimicry [22], hypoxia [23], and autophagy [24]; and (vii) metabolic adaptation [25,26,27,28].