In addition to the mutations in the signalling pathways, other adaptive mechanisms like overexpression of MITF, persistent activation of receptor tyrosine kinases, expression of NGFR, nerve growth factor receptor (also known as CD271), and phenotype switching (a phenomenon of antagonism between proliferation and invasion driven by slow-cycling cell population) seem to have important roles in the development of therapy resistance in melanoma [24,25,26,27]. The gene discussed is NGFR; the disease is melanoma.