The effects of ALK TKIs were linked to a specific inhibition of ALK activity and not to off-target effects for the following reasons: 1) we observed similar effects with two unrelated ALK TKIs (Figure 4C); 2) ALK TKIs did not modulate EMT markers in NSCLC cell lines driven by different oncogenic mutations, such as K-Ras or EGFR mutations (Supplementary Figure 3B-3C); and 3) genetic knock-down of EML4-ALK closely phenocopied the effect of ALK TKIs on E-cadherin and vimentin mRNA (Supplementary Figure 4A-4B) and protein levels (Supplementary Figure 4C). This evidence concerns the gene EGFR and non-small cell lung carcinoma.