Mechanistically, this association reflect two major disruptions in lymphocyte homeostasis during sepsis: excessive apoptosis mediated by Fas/FasL signaling, mitochondrial dysfunction, and endoplasmic reticulum stress, and impaired lymphocyte proliferation due to reduced thymic output, bone marrow exhaustion, and upregulated immune checkpoints such as PD-1/PD-L1 and CTLA-4) [17, 20, 21]. The gene discussed is FAS; the disease is Sepsis.