NRAS and neoplasm: In the context of a polyclonal tumor where a BRAF-activating mutation is subclonal in nature with the presence of BRAF wild-type subclones, BRAF inhibition might promote the growth of the BRAF wild-type population, particularly if these subclones harbor KRAS or NRAS (neuroblastoma RAS viral (v-ras) oncogene homolog) driver mutations [19].