Both aberrant ALK expression caused by ALK rearrangements [60] and ALK amplification are oncogenic driving factors of NSCLC [61]; for example, gene fusion of EMAP-like protein 4 (EML4) and ALK induced by ALK rearrangements encodes a cytoplasmic chimeric protein with constitutive kinase activity, which accounts for 3 ~ 13% of NSCLC [62, 63]. This evidence concerns the gene EML4 and non-small cell lung carcinoma.