It was found that MYC deregulation in MM resulted in the hypoxia-independent constitutive activation of HIF1α, driving the expression of vascular endothelial growth factor (VEGF) and angiogenesis [93], which could perhaps contribute to increased metabolic flexibility of MM cells due to increased oxygenation of the BM microenvironment, thereby making the tumor cells less reliant on glycolysis (Figure 1). This evidence concerns the gene VEGFA and Miyoshi myopathy.