Since the initial pro- and anti-inflammatory cytokine balance is most probably decisive for the total inflammatory outcome of a bacterial infection and the host survival [21,35,46,47], the excessive pro-inflammatory response to S. aureus infection observed in TLR2-deficient mice is thought to be due to markedly impaired IL-10 production, at least partly, and this unbalanced cytokine response ultimately results in mouse death. The gene discussed is IL10; the disease is bacterial infectious disease.