Historically, type 1 RAF inhibitors (RAFi, vemurafenib, dabrafenib and others), which selectively target monomeric BRAF V600 mutants (Joseph et al. 2010), have been ineffective for BRAF wild-type and non-V600 mutant cancers due to the paradoxical activation of ERK signaling through induction of RAF dimerization (Lito et al. 2013; Poulikakos et al. 2010). This evidence concerns the gene RAF1 and cancer.