BRAF and Miyoshi myopathy: Although others have previously shown that RAF inhibitors paradoxically activate ERK signaling in wild-type BRAF and RAS-mutated tumors [28,40–42], we here confirmed that dabrafenib (1.25 to 2.5 μM) activated p-MEK1/2 and p-ERK in both cell lines, suggesting that paradoxical activation also occurs in MM (S4 Fig).