In sharp contrast, in an acute ischemic stroke/reperfusion model, NLRP10/PYNOD was overexpressed in the penumbra zone of wild-type animals, whereas in NLRP10/PYNOD knockout mice after ischemic stroke/reperfusion the neuronal apoptosis, the activation of glial cells, and the proinflammatory agents’ levels were reduced, and the TLR-4/NF-κB signaling pathways markedly suppressed in the hippocampus. Here, NFKB1 is linked to ischemic stroke.