As well as infection‐associated preterm birth, TLR4 is implicated in sensing and amplifying amniotic fluid PAF and SP‐A, critical fetal signals that trigger parturition to coincide with fetal maturation and ability to survive ex utero,39 and a key receptor for HMGB1 and other DAMPs released by fetal membranes in response to senescence, injury and oxidative stress.40, 41 TLR4 is associated with leucocytes as well as non‐leucocytic cell lineages in the fetal membranes and so is ideally positioned to respond to the DAMPs and fetal signals in amniotic fluid. This evidence concerns the gene HMGB1 and infection.