Quantitative analysis revealed that within the ischemic core of the infarct (defined by the region of NeuN loss) there was a significant increase in the number of actinified neurons compared to control neurons defined in either sham treated mouse brains, in the stroke condition within contralateral cortex, or within ipsilateral temporal lobe cortex distant from the infarct region. The gene discussed is RBFOX3; the disease is stroke disorder.