However, this intra-tumoral hypoxia, can also result in inhibition of prolyl hydroxylase domains (PHD), leading to stabilization of the hypoxia inducible factor 1 alpha (HIF-1α) resulting in transactivation of a plethora of genes such as the pro-angiogenic vascular endothelial growth factor alpha (Vegfa), and members of the glycolytic pathway such as glucose transporter 1 (Glut1) and phosphofructokinase (Pfk) aiding tumor cell survival [2, 4]. Here, PDC is linked to neoplasm.