A possible explanation for this might be a consequence of other frequently upregulated pathways in MM, such as the WNT/β-catenin-pathway, the RAS/RAF/MEK/ERK-pathway, and the NFκB-pathway and upregulation of the anti-apoptotic proteins MCL-1 and BCL2, which have all been shown to contribute to resistance to BET-inhibition in other cancers [121,122,123,124,125,126,127]. This evidence concerns the gene RAF1 and Miyoshi myopathy.