An EML4‐ALK fusion gene generated by inversion of the short arm of chromosome 2 is observed in approximately 5% of human NSCLCs.18, 25 The EML4‐ALK fusion oncoprotein requires an N‐terminal coiled‐coil domain of EML4 which is essential for dimerization of the fusion protein and constitutive activation of ALK kinase.26 Tyrosine kinase inhibitors binding to an ATP‐binding pocket of ALK, such as crizotinib,27 ceritinib,28, 29, 30, 31 and alectinib,32, 33 have been proven their clinical effectiveness for NSCLC with genetic alterations causing aberrant ALK activation. This evidence concerns the gene EML4 and non-small cell lung carcinoma.