Since it has been demonstrated that the intestinal immune status can be translated into the central nervous system (specifically, into the meningeal compartment through cell migration of IL17γδ-T cells from the small intestine to the meninges), stroke neuroprotection can be achieved by remodeling the intestinal immune system to a more “anti-inflammatory” phenotype, consisting of an increase in regulatory T cells and a reduction in IL17 producing γδ-T cells (IL17 γδ-T cells) [65]. This evidence concerns the gene IL17A and stroke disorder.