Second, ERBB4 might act autonomously in response to the down‐regulation of the remaining receptors, as we have observed previously in Kras mice lacking EGFR [6] or as revealed in breast cancer cells, where the intracellular domain (IDC80) of ERBB4 stands in against the tyrosine kinase inhibition of other ERBB members in order to maintain oncogenic signaling [28]. This evidence concerns the gene EGFR and breast carcinoma.