Herein, we comprehensively review the metabolic factors, including glutamate and lipids, altered in PTSD comorbidity with AS and discuss the possible implications of the pathophysiology of the adenosine monophosphate (AMP)-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathways through interactions with metabolism and autophagy. The gene discussed is AKT1; the disease is post-traumatic stress disorder.