In the cellular models, we have demonstrated that genetic silencing of mdig in MM cells leads to constitutive suppression of GP130 (IL-6ST) and pro-survival regulators, STAT3 and Akt, suggesting that mdig inhibition could be a possible strategy to suppress tumor growth in IL-6-dependent MM subtypes or sensitize them to IL-6-targeted agents. The gene discussed is STAT3; the disease is Miyoshi myopathy.