MECP2 and Rett syndrome: The fact that MeCP2–CDKL5 protein–protein interactions have been shown by two independent groups, and that mutations in CDKL5 found in patients with RTT alter its kinase activity and cellular distribution (Mari et al., 2005), suggest that these naturally occurring mutations alter the MeCP2–CDKL5 interaction and point out a functional role for these molecules in RTT development.