Several molecular studies in RTT and FXS report that these molecules are targets of FMRP and MeCP2 (Darnell et al., 2011; Gulmez Karaca et al., 2018; Maurin et al., 2018; Raman et al., 2018), suggesting that impaired homeostatic plasticity in these syndromes may be mediated by deficits in Neuroligin or Neurexin. The gene discussed is MECP2; the disease is fragile X syndrome.