When the EGFR-overexpressing DFCI81 and DFCI161 pRetroX cells were treated with EGFR and MET kinase inhibitors after doxycycline induction, we observed a shift of the ERBB3-p85 interaction from single-agent crizotinib sensitivity toward EGFR/MET codependence in both cell lines, defining the ERBB3-p85 interaction as a potential mediator and predictor of oncogene dependence in EGFR-mutant NSCLC models (Fig. 6C and fig. Here, ERBB3 is linked to non-small cell lung carcinoma.