Indeed, it has been demonstrated that KRIT1 loss-of-function causes the up-regulation of c-Jun, a basic component of the dimeric redox-sensitive transcription factor AP-1, both in cellular models and human CCM tissue samples; conversely, this up-regulation can be reversed by either KRIT1 re-expression or ROS scavenging with antioxidant compounds (Goitre et al., 2014). The gene discussed is KRIT1; the disease is cerebral cavernous malformation.