Remarkably, we found that the upregulation of Nrf2, Glo1, and phosphorylated JNK (p-JNK) caused by KRIT1 loss-of-function occurs also in vivo, as shown by IHC analyses of paraffin-embedded surgically resected CCM specimens [48], suggesting that these molecular events may contribute to CCM disease pathogenesis. This evidence concerns the gene GLO1 and cerebral cavernous malformation.