Although the clinical/pathological benefits of ACE inhibitors in CCM might be partially or totally ascribed to blockade in generation of pro-fibrotic angiotensin II, these results argue against an earlier proposition that ACE inhibitor-dependent up-regulation of the BK2R pathway might aggravate infection-associated pathology (Scharfstein et al., 2000). Here, ACE is linked to cerebral cavernous malformation.