Overall, our observations that CCM3, FAM40A and FAM40B depletion all induce a similar phenotype in endothelial cells imply that CCM3 acts via the STRIPAK complex to regulate endothelial function, and thus that altering the activity of specific STRIPAK components could alleviate the symptoms in patients with cerebral cavernous malformation. The gene discussed is STRIP1; the disease is famililal cerebral cavernous malformations.