Based on the following observations that: 1) wogonin alone or in combination with bortezomib or lenalidomide strongly repressed MM-stimulated angiogenesis in vitro and in vivo, 2) wogonin markedly inhibited MM cell proliferation in vivo, and 3) wogonin dramatically inhibited expression levels of c-Myc and HIF-1α in advanced patient-derived MM cells, we propose that wogonin could be developed into a novel therapeutic agent for treatment of advanced MM. The gene discussed is MYC; the disease is Miyoshi myopathy.