In addition, we observed that brain infarct volumes, brain edema, and neurological functions after stroke were significantly alleviated by minocycline treatment in wild type mice, whereas in MCPIP1-deficient mice, minocycline treatment failed to improve these outcomes of ischemia, which indicated that MCPIP1 may participate in minocycline-induced neuroprotection in ischemic stroke. This evidence concerns the gene ZC3H12A and stroke disorder.