Previous studies have linked lesion size to the progression of CCM, as smaller lesions in the human population appear less likely to become haemorrhagic/symptomatic.2 Indeed, Krit1ieKO mice as well as Ccm2 and Ccm3‐dependent mouse models of CCM show a range of lesion size and complexity.5 There was no statistical difference in average lesion size in SU5416‐treated Krit1ieKO mice compared to vehicle control (Figure 2A), and the distribution of lesion sizes was roughly equivalent (Figure 2B). This evidence concerns the gene PDCD10 and cerebral cavernous malformation.