HIF1A and neoplasm: We have recently described a model by which mitochondria-derived signals [including mitochondria-derived reactive oxygen species (mROS) and α-ketoglutarate (αKG), a diffusible Krebs' cycle product] can directly regulate HIF-1α (which is redox-sensitive and requires αKG in its hydroxylation-driven destabilization) in cancer cells, leading to decreased paracrine angiogenic signaling in the tumor [12].