Indeed, we demonstrated that overexpression of MFF restores the intrinsic apoptosis in TRAF3-deficient human MM cells, supporting a therapeutic potential of drugs that have been developed to target mitochondrial dynamics and are being tested in other disease models, including cell permeable peptidomimetics of MFF, mitochondrial division inhibitor-1 (mdivi-1), dynasore, P110, and 15-oxospiramilactone, etc. (44, 48, 94, 95). Here, TRAF3 is linked to Miyoshi myopathy.