Up to 70% of melanomas exhibit activating mutations within the kinases BRAF gene [206,207,208,209] and approximately 15% of melanomas within NRAS gene [210,211], resulting in constitutive and sustained activation of downstream targets, RAS–MEK–ERK1/2 axis, in addition to unresponsive negative feedback mechanisms [212]. The gene discussed is BRAF; the disease is melanoma.