The analysis of somatic mutations by sequencing of the tumor genomes in 38 MM cases revealed that the mutated genes involved in NFκB activation, protein homeostasis, and histone methylation are consistent with MM biology.(62) Moreover, activating mutations of BRAF were observed in 4% of patients; this finding has immediate clinical translational implications for the use of BRAF inhibitors. Here, NFKB1 is linked to Miyoshi myopathy.