Additional genetic alterations can co-exist with a primary targetable oncogenic “driver” alteration (e.g., oncogenic EGFR, ALK, KRAS) and may help promote tumor progression and limit therapy response (Blakely et al., 2017; Kim et al., 2019; Scheffler et al., 2019; Yang et al., 2019). This evidence concerns the gene ALK and neoplasm.