TLR4-deficient mice with MyD88 knocked out were used to demonstrate that the early protection of BPZE1 might be mediated via TLR4 signal path, inducing an inflammatory response in the early stage and increased pertussis-specific antibody (and possibly T cells) responses in the later stage, all of which contributed to the clearance of B. pertussis [112]. The gene discussed is TLR4; the disease is pertussis.