Since the HER2 protein heterodimerizes preferentially with HER3 (32) – which, by virtue of numerous YXXM peptide motifs in its carboxyterminal tail (33), is a potent driver of the anti-apoptotic PI3K-AKT-mTOR pathway (34) – therapeutic inhibition of HER2-initiated signaling can be predicted to augment tumor cell kill by chemotherapy. The gene discussed is AKT1; the disease is neoplasm.