A study by Di et al. indicated that either transient expression of miR-34a synthetic mimics or lentivirus-based miR-34a-stable enforced expression inhibited growth and triggered apoptosis in multiple myeloma (MM), synthetic miR-34a downregulated the target of Bcl-2, cyclin dependent kinase 6 (CDK6), and Notch-1 at both the mRNA and protein level, while lentivirus-based miR-34a-stable also inhibited tumor growth and improved survival in mice bearing TP53-mutated MM xenografts without systemic toxicity [215]. The gene discussed is BCL2; the disease is Miyoshi myopathy.