Beta1-integrin is constitutively overexpressed in basal/HER2+ BC cells with de novo resistance to trastuzumab [21, 109], whereas the expression of a heavily N-glycosylated variant of beta1-integrin is activated during the spontaneous conversion of trastuzumab-sensitive HER2+ luminal cells to a trastuzumab-unresponsive HER2− claudin-low phenotype. The gene discussed is ERBB2; the disease is breast cancer.