In addition, within hours of systemic bacterial infection, acetate accumulates in serum, and upon uptake by memory CD8+ T cells, stress levels induced by acetate expand cellular acetyl coenzyme A via ATP citrate lyase and promote the acetylation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH), which catalyzes glycolysis while increasing GAPDH activity, thereby facilitating the response of fast memory CD8+ T cells to exert superior immune control [92]. This evidence concerns the gene CD8A and bacterial infectious disease.