The natural history of NSCLC is actually linked to the occurrence of “driver” molecular abnormalities, among which are KRAS (24%), epidermal growth factor receptor (EGFR; 15%), ERBB2 (<5%), or BRAF (<5%) gene mutations; MET amplification (<5%); MET exon 14 skipping (<5%) and ALK (<5%), ROS1 (<2%), or RET (<1%) gene rearrangements [3]. This evidence concerns the gene ROS1 and non-small cell lung carcinoma.