Chromosome translocations that lead to fusions of variable genes to the kinase domain of BRAF or CRAF have been extensively reported in cancers [22–25], while the alternative splicings that partially delete the N-terminus of BRAF(V600E) and thus enhance the dimerization of BRAF(V600E) isoforms have been shown as one of important mechanisms that underlie RAF inhibitor resistance in cancer therapy [26]. This evidence concerns the gene RAF1 and cancer.