We also treated the other ALK-rearranged NSCLC cell line characterized by an epithelial phenotype (H3122) to check whether the EMT markers, E-cadherin and vimentin, changed upon ALK inhibition and found that the level of E-cadherin expression remained stable and vimentin still undetectable for the whole period of inhibition with TKIs (Supplementary 3A), thus indicating that in this cell line ALK activity was not regulating an EMT phenotype. This evidence concerns the gene ALK and non-small cell lung carcinoma.