Furthermore, taken together with recent evidence suggesting a role for the oxidative DNA damage response gene Gadd45α in the promotion of epigenetic events by repair-mediated DNA demethylation [74], [93], [94], our finding that KRIT1 loss-of-function leads to a strong transcriptional induction of Gadd45α suggests an additional potential oxidative stress-mediated pathogenic mechanism for CCM. Here, KRIT1 is linked to cerebral cavernous malformation.