HIF1A and Miyoshi myopathy: 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).