Administration of CTRP3 reduced reactive oxygen species and malondialdehyde production, increased the level of glutathione, attenuated cerebral edema and BBB disruption, promoted angiogenesis, and improved neurological defects via both protein kinase A (PKA) and AMPK/hypoxia inducing factor‐1α (HIF‐1α)/vascular endothelial growth factor (VEGF) pathways in an intracerebral hemorrhage rat model.36, 37. This evidence concerns the gene HIF1A and intracerebral hemorrhage.