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. The gene discussed is ALK; the disease is neoplasm.