To address these gaps in our knowledge of AKT signaling related to psychiatric disorders, we selectively removed AKT isoforms from the mouse brain using complementary genetic approaches, generating mutant mice with single-isoform deficiencies in AKT1, AKT2, or AKT3; selective loss of AKT1 in forebrain excitatory neurons; or double loss of AKT1 and AKT3 isoforms. This evidence concerns the gene AKT1 and psychiatric disorder.