The activation of P53 pathways in Rett syndrome neurons has parallels in aging, and it is tempting to consider Rett syndrome as a potential early-aging syndrome, as many of the effects of loss of MECP2 overlap with phenotypes that are known to occur in aged neurons such as dendritic defects, metabolic defects, epigenetic instability, lysosomal dysfunction, or senescence. The gene discussed is TP53; the disease is atypical Rett syndrome.