ALK has previously been linked with autophagy, in glioblastoma and in crizotinib-resistant NSCLC cell lines [64, 65], however in both of these studies the ALK tyrosine kinases (the full length ALK receptor in glioblastoma, and the EML4-ALK fused oncoprotein in NSCLC) were not the direct target of the therapeutic treatment. Here, EML4 is linked to non-small cell lung carcinoma.