According to some studies, the activation of JNK and p38 contributed to LPS‐induced organ injury, whereas the inhibition of JNK and p38 improves the survival of septic mice.56 Among the diverse array of MAPKs, extensive attention has been given to p38 MAPK because of its capacity to transduce and amplify the intracellular inflammatory response.57 In the current study, we investigated the phosphorylation of p38, JNK and ERK in the mouse model of ALI and found that these protein levels were significantly reduced after PAF pre‐treatment. Here, MAPK8 is linked to acute respiratory distress syndrome.