Aberrant expression of pro-angiogenic genes (vascular endothelial growth factor [VEGF], basic fibroblast growth factor [bFGF], and hepatocyte growth factor [HGF]), and down-regulation of anti-angiogenic genes by MM cells further increase the angiogenic stimulus and explains the presence of BM angiogenesis at various degrees in all myeloma patients [5]. This evidence concerns the gene FGF2 and Miyoshi myopathy.