Conversely, it would be interesting to address whether a worsening of hepatic metabolic and redox alterations caused by KRIT1 haploinsufficiency, including an increase in the low-grade hepatic and systemic inflammatory state consequent to the dysregulated hepatic glucose metabolism and inefficient antioxidant/antiglycative defenses, may represent a risk factor for CCM disease pathogenesis. The gene discussed is KRIT1; the disease is cerebral cavernous malformation.