Given that in vitro TNF-α and IFN-γ neutralization could reverse CXCL10 elevation and that remarkably increased TNF-α, IFN-γ and CXCL10 were detected in the ischemic brains of Vdr-cKO mice, we then assessed whether combined inhibition of TNF-α and IFN-γ could likewise reduce CXCL10 production and rescue the exacerbated inflammation and functional deficits in stroke Vdr-cKO mice. The gene discussed is IFNG; the disease is stroke disorder.