The development of an endothelial-specific, temporally-inducible Krit1 knockout mouse model which recapitulates the human disease [29,30] bolstered these discoveries and revealed several potential therapeutic targets that could be inhibited to limit CCM-like lesion formation, including ROCK [31], VEGFR2 [32], and ERK5 [33]. This evidence concerns the gene KRIT1 and cerebral cavernous malformation.