The missense mutations D299G and T399I were associated with LPS hypo‐responsiveness and increased susceptibility to infection by GNB, and the underlying mechanism may be due to the fact that D299G polymorphism could damage the recruitment of MyD88 and TRIF to TLR4 and the subsequent activation of downstream signalling pathway.46 In addition, TLR4 plays a crucial role in the phagocytosis of GNB. This evidence concerns the gene TLR4 and infection.