However, previous studies reported that neamine treatment (a blocking agent of the ANG activity) was neuroprotective after stroke in a rat model of type I diabetic rats and that the failure of bone-marrow-derived cell therapy after stroke in the same model of diabetic rats was potentially linked to an increase in periinfarct and vascular ANG in infiltrating macrophages (22, 23). The gene discussed is ANG; the disease is stroke disorder.