Lung cancer (LC) is the leading cause of cancer-related mortality worldwide.1 Recently, there has been considerable advances of molecularly-targeted therapies in LC patients; epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), including gefitinib, erlotinib and afatinib, are utilized in patients with EGFR mutations, while the anaplastic lymphoma kinase (ALK) inhibitor, crizotinib, is employed in those with ALK rearrangement.2 One of the newly recognized molecular targets in LC is FGFR. The gene discussed is ALK; the disease is lung cancer.