ERBB2 and cancer: This was done because massive HER2 overexpression in cancer cells promotes ligand-independent modes of dimerization and signaling that is likely mechanistically distinct from canonical ligand-dependent modes of dimerization and physiologic signaling in cells with normal levels of HER2, and thus development of therapeutics based on the physiologic ligand-dependent modes often do not translate well to the pathologic ligand-independent signaling occurring in cancer cells.