First, small molecular tyrosine kinase inhibitors (TKIs) effectively target a growing number of gain-of-function molecular targets (i.e., driver oncogenes), such as sensitizing mutations in the EGFR, BRAF V600E, MET exon 14 skip or ERBBR2 (HER2) genes, and gene rearrangements in the ALK, ROS1, RET, MET, and neurotrophic receptor tyrosine kinase (NTRK) genes, regardless of their tumor PD-L1 expression. The gene discussed is ROS1; the disease is neoplasm.