ERBB2 and neoplasm: Activation of this receptor family induces potent signaling through the mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) pathways which promote tumor cell growth and survival.1 HER2 does not have a known ligand and exists in an “open” configuration with its dimerization interface accessible in the native state.2,3 This property makes HER2 the preferred dimerization partner of the other ERBB receptors.4 Heterodimers containing HER2 are poorly internalized and degraded, a phenomenon that is more prominent when HER2 is overexpressed.5