ROS1, ALK and c-MET, appear to be reasonable choices because the known crosstalk between EGFR signaling and all three signaling pathways, and their genetic alterations or aberrant expression may confer resistance to EGFR inhibition in NSCLC or other cancer types24, 25, 26, 27, 28, 29. This evidence concerns the gene MET and non-small cell lung carcinoma.