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. The gene discussed is AKT3; the disease is psychiatric disorder.