Kinase inhibitors (KIs) form the cornerstone of the therapeutic strategy in patients with non-small cell lung cancer (NSCLC) harboring molecular driver alterations, such as epidermal growth factor receptor (EGFR) mutations, v-Raf murine sarcoma viral oncogene homolog B (BRAF) mutations, anaplastic lymphoma kinase (ALK) fusions, ROS proto-oncogene 1 (ROS1) fusions, etc. [1]. This evidence concerns the gene ROS1 and non-small cell lung carcinoma.