Consistent with our previous findings in KRIT1 knockout cellular models and surgical samples of human CCM lesions [22,23], Western blot analysis of subcellular fractions of liver homogenates demonstrated an increased nuclear accumulation of Nrf2 in the liver of KRIT1+/− mice as compared to their WT counterparts (Figure 5a), suggesting the induction of a sustained adaptive antioxidant response. The gene discussed is NFE2L2; the disease is cerebral cavernous malformation.