In the present study, we demonstrate that ASK1 is crucial for promoting infection-induced uterine inflammation leading to preterm birth by regulating the JNK and p38 pathways, based on findings from an LPS-induced preterm birth model utilizing two independent types of ASK1-genetically-engineered mice, as well as in vitro studies using human choriodecidua, thus, implicating ASK1 as a potential therapeutic target for preterm birth. Here, MAPK8 is linked to infection.