Although successful targeting of melanomas with the BRAFV600E mutation improves overall survival, the long-term efficacy of available therapeutics, including BRAF inhibitors (e.g., vemurafenib and dabrafenib alone or in combination with mitogen-activated protein kinase (MEK) inhibitors (e.g., Trametinib and Selumetinib), are unable to cause complete tumor regression [8,9]. The gene discussed is BRAF; the disease is neoplasm.