Nonetheless, despite these observations and work demonstrating that IL-1β is integral to the anhedonic and anti-neurogenic effects of stress (Koo and Duman, 2008), most evaluations of the protective effect of antidepressants in both animal and cellular experiments have modeled depression using stress paradigms or glucocorticoid exposure to simulate stressors. The gene discussed is IL1B; the disease is major depressive disorder.