Since various stress conditions leading to proteasome inhibition or overload are described to be associated with enhanced NFκB transcription factor activity, and since NFκB can stimulate HSPB8 and BAG3 expression [42,77], we checked NFκB activity in control and DMD myoblasts and observed an increased level of the RelA/p65 subunit of NFκB, whereas the level of IκBα, the inhibitory subunit of the transcription factor was not modified. Here, NFKB1 is linked to Duchenne muscular dystrophy.