In summary, it may be suggested that, during PTSD, a dysfunctional HPA axis increased CRH to stimulate adrenocorticotropin secretion, leading to an imbalance in cortisol level that alters synaptic plasticity, activating NF-κB signaling and releasing proinflammatory cytokines. This evidence concerns the gene NFKB1 and post-traumatic stress disorder.