Similar endogenous labeling strategies of other synaptic proteins would be useful to investigate the molecular mechanisms of nearly any behavior, including GluA1-independent forms of plasticity (Frey et al., 2009) or disease models that display synaptic pathologies, such as SynGAP haploinsufficiency or Alzheimer’s disease (Gamache et al., 2020; Sheng et al., 2012). This evidence concerns the gene SYNGAP1 and early-onset autosomal dominant Alzheimer disease.