Given the evidence that PGC1α can protect against apoptosis induced by hyperthermia in vitro (Figure 5) and that liver and kidney are the primary loci affected during heat stroke in humans,24 we analyzed WT and PGC1α KO mice and showed increased apoptosis, increased cytosolic cytochrome c (CytC) release from mitochondria and elevated caspase-3 activity in these two organs in PGC1α-null mice after heat shock (Figures 6b–f). Here, CYCS is linked to Heat Stroke.