This review examines the major mechanisms underlying lymphocyte function inhibition in sepsis and organizes them into interconnected pathways, including inhibitory membrane receptors (such as PD-1, CTLA-4, and LAG-3), mitochondrial and endoplasmic reticulum stress-related organelle dysfunction, exosome-mediated intercellular communication, non-coding RNA regulatory networks, and cytokine-driven immune modulation. The gene discussed is CTLA4; the disease is Sepsis.