Both ALK mRNAs and proteins are highly expressed in these EML4-ALK positive carcinomas (Figures 3 and 4), which is consistent with the notion that EML4-ALK rearrangements cause aberrant expression of EML4-ALK fusion oncogene and overactivation of ALK tyrosine kinase, which in turn leads to the inhibition of apoptosis and promotion of tumor cell proliferation [25, 29, 30]. This evidence concerns the gene ALK and carcinoma.