Importantly, miR-29b levels were significantly reduced in MM dendritic cells, and its reconstitution counteracted pro-inflammatory pathways in co-cultured MM cells, including signal transducer and activator of transcription 3 and nuclear factor-κB, and cytokine/chemokine signaling networks, which correlated with patients’ adverse prognosis and development of BD. The gene discussed is STAT3; the disease is Miyoshi myopathy.