Indeed, the clinical efficacy of all ALK inhibitors is the eventual development of multidrug resistance because of the selection pressure of the treatments on NSCLC cells.17 Such resistance can be attributed to the occurrence of secondary mutations in the ALK tyrosine kinase domain, amplification of ALK, drug efflux pumps, activated bypass signaling pathways, lineage changes, and primary ALK-tyrosine kinase inhibitor (TKI) resistance.17 The gene discussed is ALK; the disease is non-small cell lung carcinoma.