This conclusion is supported by the results showing that: (i) the expression of MEF2D prominently decreased in the hippocampus of rats after brain I/R injury; (ii) MEF2D silencing increased the infarct volume of ischaemic stroke rats and decreased the neurological impairment and short‐term survival rate of rats after stroke by exacerbating apoptosis; and (iii) MEF2D silencing increased cognitive dysfunction in ischaemic stroke rats. The gene discussed is MEF2D; the disease is Stroke.