JUN and cerebral cavernous malformation: Remarkably, experimental support that synergistic oxidative stress and inflammatory responses are indeed implicated in CCM disease pathogenesis was provided by the finding that the redox-sensitive up-regulation of c-Jun induced by KRIT1 loss-of-function was accompanied by the induction of COX-2, a major inflammatory mediator involved in vascular dysfunction (Goitre et al., 2014) (see Section 3).