Recently, it has been proved that toll-like receptors like TLR2, TLR4 and TLR5, the myeloid differentiation primary-response protein 88 (MyD88), and the nuclear factor-kappa B (NF-κB) activation as mechanisms linking the pathogenesis of ischemic stroke.23 Activation of TLRs causes increased proinflammatory cytokine expression, such as interleukin-17 (IL-17) and interleukin-23 (IL-23). Here, NFKB1 is linked to ischemic stroke.