Interestingly, the involvement of AP4 in AMPAR exocytosis could potentially explain the intellectual disability phenotype of AP4 deficiency syndrome; an imbalance between GluA2 and GluA1 subunits in the composition of AMPARs was previously shown to cause changes in how neurons respond to synaptic plasticity events, thus impacting on learning and memory functions (Moretto et al., 2018). The gene discussed is GRIA1; the disease is Intellectual disability.