This signaling is ERBB2-specific and appears not to depend on ERBB2 heterodimers as in the context of the breast cancer cell line used here (expressing negligible ERBB4 levels), silencing of EGFR and ERBB3 does not impair the ERK-dependent AKT de-phosphorylation elicited by Abs. The gene discussed is ERBB4; the disease is breast cancer.