Cerebral hemodynamic dysregulation, leading to increased cerebral capillary pressures and depression of normal cerebral vascular auto-regulation, likely plays an important role in the development of cerebral edema.[3] However, these factors alone are not considered sufficient,[4] and additional neurohumoral mediators are believed to play a prominent role in the development of increased capillary permeability.[1] Speculation has focused on several possible mediators, most notably inducible nitric oxide synthase (iNOS) and vascular endothelial growth factor (VEGF). Here, VEGFA is linked to brain edema.