EML4 and non-small cell lung carcinoma: In contrast to previous reports in ALK+ NSCLC [56–58] along with our EML4-ALK in vitro assay, we observe resistance to alectinib, which is more in agreement with this mutation favoring ATP binding over inhibitor binding, and suggests potential differences in the conformational changes induced by a leucine substitution at this residue based on ALK's fusion partner.