A previous report indicated that ANGPTL2 derived from retinal cells or macrophages leads to leukocyte adhesion, infiltration, and expression of pro-inflammatory cytokines such as TNF-α in the acute phase of endotoxin-induced uveitis.[8] Here, we provide additional evidence that ANGPTL2 functions in acute cerebral ischemia and worsens neurological deficits, increases infarct volume, and promotes expression of neurotoxic inflammatory cytokines, including TNF-α and IL-1β (Fig 6). The gene discussed is TNF; the disease is uveitis.