Cerebral cavernous malformations (CCM) are a leading cause of childhood stroke, and familial cases are linked to mutations in genes regulating blood vessel development and integrity. Glading and Ginsberg show that one of these genes, KRIT1, controls the subcellular distribution of the multifunctional protein β-catenin. Loss of KRIT1 drives β-catenin into the nucleus, activating multiple vasculogenic genes. In a further twist, reducing KRIT1 expression in mice that are prone to colon cancer increases adenoma formation, suggesting a wider role for CCM proteins in cancer.

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