For oxidative (but not Warburg-type) tumors, physiological millimolar lactate levels were found to inhibit the prolylhydroxylase domain 2 (PHD2)-driven hydroxylation and subsequent degradation of HIF-1α, thus aiding in the activation of HIF-1 signaling, VEGF secretion and tumor angiogenesis even in normoxic compartments of the malignant mass [50]. Here, HIF1A is linked to neoplasm.