As outlined in this review, and in addition to mismatch repair deficiency/microsatellite instability and tumor mutational burden (the discussion of which was beyond the scope of the manuscript), mutations of KRAS and BRAF, overexpression/amplification of HER2, and fusions of NTRK, ALK and ROS1 provide an opportunity for novel therapeutic approaches with interesting, and in some cases unprecedented, results. Here, ROS1 is linked to neoplasm.