Overwhelming evidence has shown that type 1 diabetes (T1D) impairs endothelial nitric oxide synthase (eNOS)‐ and neuronal nitric oxide synthase (nNOS)‐dependent dilation of cerebral arteries and arterioles via mechanisms that appear to favor oxidant‐producing over antioxidant‐protecting pathways (Mayhan 1989; Mayhan et al. This evidence concerns the gene NOS3 and type 1 diabetes mellitus.