Furthermore, the increased expression of receptor tyrosine kinases (RTK) like PDGFRB (Platelet derived growth factor receptor beta), EGFR (Epidermal growth factor receptor), MET (c-Met or hepatocyte growth factor receptor), and AXL (AXL receptor tyrosine kinase), which are induced due to the high phenotypic plasticity of melanomas and driven by diverse transcription factors, are correlated with reduced drug responsiveness7–10. This evidence concerns the gene MET and melanoma.