A meta‐analysis showed that TLR4 A299G polymorphism was significantly associated with the susceptibility to pneumonia.43 It was reported that LPS O‐polysaccharide and T2SS mutant‐induced responses depended on TLR4‐MyD88 activation, suggesting LPS O‐polysaccharide and PulA T2SS as potential targets for designing antimicrobials.24 In addition, TLR4 mutant mice were more susceptible to butylated hydroxytoluene (BHT)‐induced pneumonia than TLR4 wild‐type mice. The gene discussed is MYD88; the disease is pneumonia.