Importantly, IHC analysis of distinct CCM surgical specimens from KRIT1 loss-of-function mutation carriers demonstrated that an increased accumulation of S-glutathionylated proteins occurs also in endothelial cells lining the lumen of abnormally dilated CCM vessels, compared with perilesional normal vessels, thus providing clinical relevance to the in vitro results and suggesting a potential correlation with CCM disease progression and severity [51]. The gene discussed is KRIT1; the disease is cerebral cavernous malformation.