KRIT1 and cerebral cavernous malformation: Taken together with the findings in cellular models, the outcomes of IHC analyses on surgical samples of human CCM lesions suggest that the observed enhanced protein S-glutathionylation could be part of an abnormal adaptive response to altered redox homeostasis and signaling caused by KRIT1 loss-of-function, thus representing a novel pathological signature in CCM disease that might be developed for diagnostic and therapeutic strategies in the future.