Remarkably, in light of our new findings, it is also tempting to hypothesize that the pathological phenotypes observed in endothelial-specific conditional knockout mouse models upon postnatal deletion of KRIT1, including the stochastic, spatially and temporally restricted development of vascular lesions mimicking human CCM lesions [87,88] and the crucial contribution of proinflammatory metabolites produced by the gut microbiome [38], could be exacerbated by a diet enriched in fructose, leading to vascular complications and death at an earlier age. The gene discussed is KRIT1; the disease is cerebral cavernous malformation.