While studies using informative in vitro and in vivo models to consider the proper cellular context are needed to dissect in deeper detail the molecular pathways involved in RMNS, the present findings suggest that dysregulation of these genes (and/or other genes whose expression in neuronal cells is controlled by HIST1H1E-mediated regulation of chromatin organization) may contribute to neurogenesis defects and/or abnormalities of synaptic plasticity in patients with RMNS. This evidence concerns the gene H1-4 and Rahman syndrome.