For example, it was confirmed to be involved in resistance to complement-mediated killing [33,34] and complement C3aR/C5aR-mediated monocytes chemotaxis [35]; it was also the main stimulus for TNF-α production independently of its membrane perforation ability [36] and was involved in the invasive infection and virulence of S. suis [37–40]. The gene discussed is TNF; the disease is infection.