CCMs can occur in a sporadic or autosomal dominant fashion (Familial cerebral cavernous malformations, FCCM), and the latter tends to have multiple lesions as a consequence of inherited loss-of-function genetic variants, predominantly in any of the KRIT1/CCM1 (Krev interaction trapped 1), MGC4607/CCM2 (cerebral cavernous malformation 2), or PDCD10/CCM3 (programmed cell death protein 10) genes (2–4). The gene discussed is KRIT1; the disease is famililal cerebral cavernous malformations.