First indications suggesting a functional interdependence of L1 and MeCP2 were gained by studying reprogrammed human stem cells from a Rett syndrome individual: reduced L1 expression as well as reduced neurite outgrowth and neuronal cell survival were observed, and expression of wild-type MeCP2 in these cells resulted in increased L1 levels, neurite outgrowth, and neuronal cell survival [9]. Here, MECP2 is linked to atypical Rett syndrome.