Since RAS is shown to exert dominance over downstream MAPK members in activating the pathway in cancer cells [48], and RAS mutations are known to accentuate the allosteric MAPK activating effects of BRAFi’s in BRAF WT MM cells [49], activating codon 12 RAS mutations may potentially be biomarkers of efficacy for MTX + dabrafenib combination treatments independent of BRAF mutational status. Here, BRAF is linked to cancer.