ERBB2 and neoplasm: In a mouse model of HER2+ breast cancer, i.e., MMTV-Neu (Neu), which express an activated rat ErbB2/HER2 homologue selectively in the mammary gland [31], tumor onset, growth, and metastasis were suppressed by blocking Gi/o-GPCR signaling, either via a catalytic subunit (the A-protomer) of pertussis toxin (which selectively uncouples Gi/o proteins from their cognate receptors) or inhibitors that target the PI3K/AKT and Src downstream effectors [23].