The reverse is also true, as only adult deletion of Camk2a completely phenocopies the deficits observed in germline knockout mice (Achterberg et al., 2014), whereas adult deletion in other NDD models do either not or only partially copy the observed behavioral abnormalities (e.g. upon Syngap1, Mecp2, or Ube3a deletion; Gemelli et al., 2006; Ozkan et al., 2014; Sonzogni et al., 2019), or only show the phenotypes upon juvenile deletion (e.g. upon Ube3a deletion; Sonzogni et al., 2019), proving a critical window for protein expression of this gene. The gene discussed is MECP2; the disease is Neurodevelopmental delay.