Taken together, our findings clearly provide new insights suggesting that stem-like properties can be a pivotal driver of EML4-ALK-mediated tumorigenicity of NSCLC cells and inhibition of mTOR signaling can be a potential strategy to clinically control intractable stem-like phenotypes of EML4-ALK+ NSCLC. This evidence concerns the gene EML4 and non-small cell lung carcinoma.