PRRT2 and Duchenne muscular dystrophy: Moreover, we show that lack of PKCθ prevented the hyper-activation of the pro-inflammatory pathways NFkB and AP1, known to be up-regulated in mdx. It is worth noting that chronic activation of NF-kB signalling is required for DMD pathology by acting both on immune cells and damaged skeletal muscles to promote inflammation and to inhibit myogenic differentiation of muscle precursors [29].