The dysfunction of SLC39A8 had an impact on alterations in glutamate and immune function, for example, a reduction in GluN2A and GluA1/2/3 receptor surface expression, decreased BBB integrity, and increased IL-6/IL-1β protein expression (53), which may indicate that the occurrence of DCC and MDD, and LCU and insomnia is medicated by glutamate signaling and altered immune and inflammatory signals (54, 55). This evidence concerns the gene IL1B and insomnia.