In fact, S100B engages RAGE in endothelial cells thereby activating NF-κB transcriptional activity, increasing expression of vascular cell adhesion molecule-1, inducing monocyte chemoattractant protein-1 and RAGE transcripts and abrogating sodium nitroprusside-potentiated vasodilatation in response to ACh in endothelial dysfunction in type II diabetic (Leprdb) mice. Here, AGER is linked to endothelial dysfunction.