Mouse models support this hypothesis as while KRIT1−/− mice exhibit general developmental arrest after E9.5 and die by E11 with severe vascular defects associated with abnormal angiogenenic remodelling, including vascular dilations related to altered arterial fate and elevated endothelial mitosis [43], heterozygous KRIT1 knockout mice do not normally recapitulate CCM disease phenotypes [42]. The gene discussed is KRIT1; the disease is cerebral cavernous malformation.