Specifically, in the mesenteric arterioles of the MeCP2+/− female mice, we observed a dramatic reduction in the vascular response to acetylcholine, an endothelium-dependent vasodilator, together with a preserved relaxation to sodium nitroprusside, a direct smooth muscle cell relaxant compound, indicating the presence of endothelial dysfunction. This evidence concerns the gene MECP2 and endothelial dysfunction.