Kristin Bergethon et al. found that ROS1 rearrangement may be a new NSCLC typing. The study screened 1073 lung cancer specimens from four centers for the presence of ROS1 or ALK rearrangements by FISH. The results found that 1.7% (18/1073) had ROS1 rearrangements and 2.9% (31/1073) had ALK rearrangements. Positive patients were younger and almost never smoked compared to ROS1-negative patients (p<0.001), and all ROS1-positive patients had adenocarcinoma, which tended to be highly differentiated, but there were no significant differences in overall survival for patients yet, regardless of whether ROS1 rearrangement occurred. Shaw reported the preliminary efficacy of crizotinib in patients with ROS1-positive NSCLC at the 2012 ASCO Annual Meeting. The study enrolled 15 patients with a median age of 54 years, all with adenocarcinoma, and 12 patients had received ≥1 prior antitumor therapy. Fourteen cases are currently evaluable for efficacy, and 12 patients remain on treatment. The median duration of treatment was 26.0 weeks, with an effective rate of 57.1% (8/14, 7 PR, 1 CR) and an 8-week disease control rate of 79%. In addition to mild visual disturbances, the most common adverse reactions (≥10% of patients) were transient elevated liver enzymes, diarrhea, angioneurotic edema, abnormal taste, nausea, vomiting, neutropenia, and sinus bradycardia. grade 3 toxicity was observed in 4 patients: neutropenia, hypophosphatemia, elevated alkaline phosphatase, and elevated ALT. Although ROS1 rearrangement suggests a new subtype of NSCLC, its normal function is not well understood. At the cellular level, ROS1 activates signaling pathways that share receptors with other tyrosine kinases. In tumor patients, chromosomal rearrangements are the primary mechanism of ROS1 activation, and the proto-oncogene form of ROS1 is seen to activate downstream signaling pathway substances associated with malignant tumor formation. Therefore, it is tentatively suggested that the ROS1 gene may be involved in the process of lung carcinogenesis and, in turn, a therapeutic target for Crizotinib because of its rearrangement.