,12 Elevated abundance of HIF1-α targets adrenomedullin and vascular endothelial growth factor (VEGF) within MM plasma cells, and VEGF and HLA-G in patient sera provide further evidence of BM hypoxia.13, 14, 15 Moreover, MM plasma cell proteomes exhibit features of hypoxic adaptation,16 and hypoxia-activated prodrugs demonstrate clinical activity, implying activation within the BM.17 This evidence concerns the gene HLA-G and Miyoshi myopathy.