Collectively, caspase-8-mediated post-translational Sp1 degradation appears to be among major mechanisms of the synergistic anti-MM effects by panobinostat and proteasome inhibitors in combination, aside from the induction of direct caspase-8 and caspase-9-dependent apoptosis [20, 21], and potentiation of ER stress [3]. The gene discussed is CASP8; the disease is Miyoshi myopathy.