In vivo, loss of heterozygosity for either CCM3/PDCD10 or GCKIII produces vessels with narrowed or irregular lumina, accompanied by dilation of adjacent microvascular segments, strikingly reminiscent of the cavernous, thin‐walled architecture characteristic of CCM lesions (Chan et al. 2011). This evidence concerns the gene PDCD10 and cerebral cavernous malformation.