TNF-α was reported to be primarily released by microglia and peaked at 12–24 h following ischemic stroke, where it bound its cognate receptors and killed neuronal cells directly.[11] iNOS was the main rate-limiting enzyme of nitric oxide production under inflammatory states and was generally known to be neurotoxic.[19] IL-1β was also shown to aggravate neuroinflammation as an amplifier of the inflammatory cascade. Here, TNF is linked to ischemic stroke.