Several of the aforementioned agents downstream of HIF-1 are also potent inflammatory mediators, and recent studies have shown that HIF-1 plays a central role in stress responses beyond hypoxia (reviewed in [25, 28] ). Many pro-inflammatory cytokines and reactive oxygen species (ROS) can activate HIF-1 even under normoxic conditions [25, 37] , with subsequent HIF-1 induction of proteins that promote inflammation in a seemingly positive feedback loop of inflammation regulation (reviewed in [28, 38] ). HIF-1 has also been shown to be essential for the regulation of the glycolytic capacity of myeloid cells. In the absence of HIF-1, the cellular ATP pool is drastically reduced, and this metabolic defect causes profound impairment of macrophage and neutrophil cell aggregation, motility, invasiveness, and antimicrobial activity [24] .