Though the underlying molecular mechanisms for oxidative stress induced p38 MAPK activation remain elusive, it is suggested by Williams, A. S. et al. that the Toll-like receptor (mainly TLR4 and TLR2) signaling pathways may be involved, as the p38 MAPK-mediated ozone-induced airway hyperresponsiveness was blocked by genetic inhibitions of TLR4 and TLR2 in mice [33]. Here, TLR4 is linked to airway hyperresponsiveness.