We can hypothesise that when HER2+ breast cancer has already been treated by co-inhibition of heterodimerization partner HER3 by the use of pertuzumab and developed resistance, then another partner of the HER2 receptor, EGFR, may be overexpressed as a compensatory mechanism to the therapeutics, in which case, an anti-EGFR inhibitor maybe more effective compare to lapatinib. The gene discussed is ERBB3; the disease is breast cancer.