Preclinical models of acquired resistance to EGFR-TKIs in EGFR-mutated NSCLC cells showed that the concomitant inhibition of both SMO and MET led to significant antiproliferative and proapoptotic effects, as well as the loss of the mesenchymal phenotype, suggesting new combination strategies [154]. This evidence concerns the gene MET and non-small cell lung carcinoma.