In BRAF mutant melanoma, resistance to BRAF and MEK kinase inhibitors has also been associated with phenotype plasticity and gene expression program alterations, which identify three different cellular states: a pigmented melanocytic state associated with transcription factor MITF expression; a neural crest-like state characterized by nerve growth factor receptor (NGFR) activation; and an undifferentiated state characterized by low levels of the transcription factor SOX10 and high levels of receptor tyrosine kinases, such as AXL and the epidermal growth factor receptor EGFR [112]. This evidence concerns the gene EGFR and melanoma.