An increase in blood LPS levels (“endotoxemia”) activates the immune system, triggering the release of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), which can cross the blood–brain barrier, leading to neuroinflammation, HPA axis activation, and behavioral symptoms, such as anhedonia, anxiety, and low mood, resembling depression or post-traumatic stress disorder (PTSD), as demonstrated in animal studies wherein LPS induced depression- and anxiety-like behaviors [46]. The gene discussed is IL1B; the disease is major depressive disorder.