Frequent mutationsin the pathway, primarily generating activated forms of RAS and BRAF,are observed in more than 30% of human cancers.21,22 The canonical pathway integrates extracellular signals through transmembranereceptors, switches Ras GTPase to the active GTP-bound form, and recruitsRAF kinases to the membrane, where they are activated.23 Three RAF protein kinase (A, B, and C) serveas effector kinases in the RAS-ERK signaling cascade. This evidence concerns the gene BRAF and cancer.