Previous experimental data showed that bacteria can induce M1 macrophages to produce a large amount of proinflammatory mediators, including Tumor necrosis factor-α (TNF-α), Interleukin-1(IL-1), and Nitric oxide (NO), via the TLR2 signalling pathway during the early and acute stages of bacterial infection (Khan et al., 2015). The gene discussed is TLR2; the disease is bacterial infectious disease.