In EML4-ALK(+) NSCLC, gain in ALK copy number, loss of ALK gene rearrangement and engagement of other cell signaling pathways mediated by increased phosphorylation of EGFR, amplification of KIT or KRAS mutations have also been implicated in the development of acquired resistance to crizotinib. This evidence concerns the gene EML4 and non-small cell lung carcinoma.