It was found that protein kinase B (AKT), glycogen synthase kinase 3 (GSK3), and eukaryotic initiation factor 4E (EIF4) pathways involved in depression were upregulated in cells after GPR56 agonists treatment such as peptides P7 “TYFAVLM-NH2” and P19 “TYFAVLMQLSPALVPAELL-NH2” [72]. This evidence concerns the gene AKT1 and depressive disorder.