In efforts to understand the molecular pathways involved in the development of pulmonary lymphoepithelioma-like carcinoma, a number of studies have examined the mutation status of classic lung cancer oncogenic driver and tumor suppressor genes, including EGFR, KRAS, BRAF, ALK, ROS1, and TP53 [4]; however, all of these common oncogenic drivers were often not mutated, indicating the involvement of other pathways in its tumorigenesis [4, 6, 7, 15, 23, 24]. This evidence concerns the gene ALK and carcinoma.