Our experimental data recapitulated their major findings and showed some novel findings: 1) the inborn deletion of Pten in the hippocampal DG was sufficient to cause severe epilepsy in adulthood; 2) the hyperactive mTOR signaling pathway disrupted Crh-ACTH homeostasis in the hippocampus; and 3) postnatal treatment with rapamycin not only reversed the seizure phenotype, but also corrected the molecular phenotypes of the excessive production of ASD-associated proteins, such as Shank3 and Homer. The gene discussed is POMC; the disease is epilepsy.