Of note, the activation of MET by HGF has been suggested as a potential mechanism of acquired tyrosine kinase inhibitor (TKI) resistance to gefitinib in epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer (NSCLC) (Yano et al., 2008) and to vemurafenib itself in BRAF-mutant melanoma (Wilson et al., 2012). This evidence concerns the gene HGF and melanoma.