In agreement with this notion, our results showed that an exposure of CPS or an infection of M. ovipneumoniae significantly induced the upregulation of MyD88 and its downstream effectors including IRAKs, TRAF6 and TAB1, therefore indicating that a MyD88-dependent pathway might be at least in part involved in the CPS- or M. ovipneumoniae-induced inflammation. The gene discussed is TAB1; the disease is infection.