In conclusion, our findings demonstrated that during OVVs infecting the tumor cells and eliciting the tumor specific oncolysis, enforced expression of miR-34a and Smac by VV-miR-34a and VV-Samc induced significant apoptosis in MM cells through blocking function of Bcl-2, and thus activating the release of cytochrome c from the mitochondrial endomembrane and finally synergistically enhancing the Smac-induced cytochrome c/Apaf-1/Caspase-9 signaling cascade (Fig. 5). The gene discussed is BCL2; the disease is Miyoshi myopathy.