Indeed, inducible KRIT1 knockout mouse models, generated by Cre recombinase technology, have proven useful for understanding mechanisms of CCM lesion genesis and testing therapeutics, as CCM lesions develop reproducibly around postnatal day 6 (P6) upon tamoxifen-mediated induction of KRIT1 deletion at P1 [89,90]. This evidence concerns the gene KRIT1 and cerebral cavernous malformation.