Our study suggested that enhanced activation of NF-κB-signaling pathway in MCPIP1-deficient mice leads to increased proinflammatory cytokine production after brain ischemia with minocycline treatment and that MCPIP1 is involved in minocycline-treatment-induced inhibition of the NF-κB-signaling pathway after ischemic stroke. This evidence concerns the gene ZC3H12A and ischemic stroke.