Melanoma is treated with a combination of surgery, traditional cytotoxic chemotherapy, targeted therapies, and immune-based therapies. Five year survival rates for patients with metastatic disease, unfortunately, are below 10% (Jemal et al. 2010). Novel therapies and treatment strategies are needed.
 Historically, melanoma has been classified according to pathological and clinical characteristics such as histology (depth, Clark level, ulceration) and anatomic site of origin. Over the past decade, it has become evident that subsets of melanoma can be further defined at the molecular level by recurrent 'driver' mutations that occur in multiple oncogenes, including BRAF, GNA11, GNAQ, KIT, MEK1 (MAP2K1), and NRAS. Such 'driver' mutations lead to constitutive activation of mutant signaling proteins that induce and sustain tumorigenesis.

​Mutations in BRAF, GNA11, GNAQ, KIT, MEK1 (MAP2K1), and NRAS can be found in approximately 70% of all melanomas. In addition, mutations in CTNNB1 have also been described in melanoma. These mutations are seldom found concurrently in the same tumor. The distribution of mutation varies by site of origin and also by the absence or presence of chronic solar damage. Importantly, targeted small molecule inhibitors are currently available or being developed for specific molecularly defined subsets of patients with melanoma.