Notably, human CCM lesions have been shown to exhibit increased expression of VEGF, supporting the idea that VEGF may play a role in the pathogenesis of this disease,8, 9 as has been suggested for other types of vascular malformations, including hereditary haemorrhagic telangiectasia.10, 11 Furthermore, the abnormal morphology and increased permeability of CCM lesions is highly similar to that seen when VEGF is overexpressed in vivo.12, 13 Our previous work using an endothelial cell‐based tissue culture model showed that loss of Krit1 and Ccm3 stimulated the expression of VEGF. The gene discussed is PDCD10; the disease is cerebral cavernous malformation.