Oncogenic alterations such as mutations in EGFR, KRAS, BRAF, and ERBB2; translocations involving ALK, ROS1, and RET; and amplifications of MET and FGFR1 in both adenocarcinoma (ADC) and squamous cell carcinoma (SCC) have provided new therapeutic avenues and enabled recognition of molecular subsets that can predict treatment response (11,12). The gene discussed is ALK; the disease is adenocarcinoma.