In order to elucidate the transcriptional programmes related to BRAF activation in MM, we used vemurafenib (a BRAF inhibitor that has recently proved to be a promising anti-myeloma drug in clinical settings) [7] to inhibit BRAF activity in U266 cells which carry the K601N mutation and showing constitutive activation of MEK/ERK signalling (Supplementary Figure 2D). Here, BRAF is linked to Miyoshi myopathy.