Together, these data suggest that, in trastuzumab-sensitive HER2+ breast cancer, components of the RAB5/RAB7A/GDI2 subnetwork are recruited to sites of αVβ6 engagement and coordinate HER2 endocytosis, signaling, and intracellular trafficking, thus modulating HER2 bioavailability at the plasma membrane (Fig. 7A). The gene discussed is ERBB2; the disease is breast cancer.