These data strongly support that JunB-mediated AF generation and secretion contributes to MM BM angiogenesis; and that inhibition of tumor growth, as evidenced by a significant decrease of Ki67 staining (Supplementary Fig. 13 [21]) by JunB knockdown, is mediated, at least in part, via antiangiogenesis. The gene discussed is MKI67; the disease is atrial fibrillation.