Consequently, mutations in any of the AP-4 subunits would presumably have similar downstream effects on vesicular glutamate receptor transport and neurotransmission, resulting in similar clinical presentations (e.g., altered neuronal excitability and risk of developing infantile febrile seizures in both AP4B1- and AP4M1-related phenotypes). The gene discussed is AP4M1; the disease is Febrile seizure (within the age range of 3 months to 6 years).