Increased promoter methylation of autistic candidate genes such as RORA, BCL2 and MECP2 are shown to be associated with reduced expression of these genes in autistic patients [2,19,62]. Treatment with decitabine was shown to demethylate promoters and restore/induce the expression of the silenced RORA and BCL2 in autistic and patients with fragile X syndrome and hence, the use of DNA demethylating agents in drug therapy for autism and fragile X syndrome has been suggested [61,62]. A similar strategy to restore/induce MeCP2 expression might be extended to treat such diseases associated with reduced MeCP2 expression, including autism and RTT. Providing insights on such therapeutic strategies, the application of epigenetic drug therapy to induce non-mutated copy of MECP2 expression in Rett syndrome cell lines has been suggested and attempted previously [65]. Therefore, our findings on the ability of decitabine to induce MeCP2 expression in differentiating NSC provide further insights on designing possible drug therapies for autism. Even though the exposure of RTT cell lines (fibroblasts) to lower doses of decitabine for a longer period did not activate MECP2 expression [65], our results
