EGFR and neoplasm: Engagement of multiple proto-oncogenes including KRAS/HRAS as a bypass mechanism of resistance to ALK inhibitors has been reported by CNA analysis in tumor biopsies by McCoach et al.9, and, in concordance with our results, the authors found multiple gains in EGFR, FGFR1, and NTRK1. Activation of ERBB2 (HER2) has been reported as a potential off-target mechanism of resistance to crizotinib in ALK-rearranged tumors40.