TRAF3 and Miyoshi myopathy: Altogether 17/88 (20%) of the MM tumors analyzed had outlier expression of Map3k14. The majority of the LTR insertions result in the elimination of exon 2 encoding the TRAF3 interacting domain known to be important for Map3k14 protein stability, as we and others previously noted in human MM, and cause constitutive NFkB activation, reflected by a high NFkB index by gene expression (Fig. 4B)25,26.