ALK and neoplasm: This finding suggested that while the sequential use of second-generation ALK inhibitors may successfully addressed deficiencies about the potency and tissue concentration of crizotinib; multiple factors leading to drug resistance can shortly come into play including ALK kinase domain solvent-front, gatekeeper and compound mutations [14, 29] and the emergence of ALK independent tumor clones that conferred non-ALK resistance mechanisms [30, 31].