Moreover, mice with a deletion of either the sGCalpha-1 or beta-1 gene are hypertensive16 and any hypertensive mouse will show a higher susceptibility to a worsened outcome in experimental stroke; however, at the same time we know that all tested anti-hypertensives were unsuccessful or dangerous in stroke therapy.17 Finally, NO, the specific stimulator of sGC, is toxic in stroke18 precluding its use and sGC as a therapeutic target. This evidence concerns the gene SGCB and stroke disorder.