It has been reported that in ischemic stroke, energy metabolism disorders and mitochondrial dysfunction may lead to the formation of large amounts of free radicals, mediate oxidative damage to DNA, inhibit antioxidant enzyme activity, upregulate Bax levels, downregulate Bcl-2 levels in astrocytes, and finally, suppress the activation of Caspase-3, thus inducing neuronal apoptosis [28]. This evidence concerns the gene BAX and ischemic stroke.