In the acute phase of ischemic stroke, pro-inflammatory cytokines damage neurons and glial cells and worsen neurological deficits.[2] IL-1β promotes immune cell migration and exacerbates disruption of the BBB and neuro-inflammation.[10] Macrophage-derived TNF-α also promotes additional inflammation by recruiting inflammatory cells,[11] thereby inducing neuronal apoptosis through TNF-related apoptosis inducing ligand.[3] Decreases in these neurotoxic effects may mediate favorable neurological outcomes observed in the ischemic brain of Angptl2 KO mice. Here, ANGPTL2 is linked to ischemic stroke.