BRAF and neoplasm: BRAF point mutations cluster in a specific region and usually result in a single phosphomimetic substitution in the kinase‐activation domain (V600E) that confers constitutive activation of BRAF and leads to uncontrolled, constitutive activity of downstream signaling pathways that stimulate cellular proliferation and increase tumor cell invasion, metastatic potential, and resistance to apoptosis (Chin, 2003; Pritchard and Hayward, 2013).