The therapeutic landscape of NSCLC has been transformed by the discovery of recurrent, targetable genomic alterations—most commonly involving EGFR, ALK, ROS1, BRAF, MET, RET, KRAS, and NTRK genes—together with the emergence of immune-checkpoint inhibitors guided by PD-L1 expression and tumor mutational burden (TMB) [5,6,7]. This evidence concerns the gene ALK and non-small cell lung carcinoma.