Since myocardium development is altered in a similar manner upon loss of CCM proteins in zebrafish15,16, and given that we found Slc39a8 to be down-regulated in Krit1/Ccm1 mouse BMECs (Fig. 6c), it is possible that aberrant zinc regulation plays a role in the development of CCM lesions. This evidence concerns the gene KRIT1 and cerebral cavernous malformation.