Furthermore, in the presence of pathogenic infection or the stimulation of danger signals, the occurrence of preterm PROM relies on fetal membrane cells initiating classical and/or nonclassical pathways of cell apoptosis.[26,27] In these pathways, the activation of Caspase-1 and Caspase-3 promotes the maturation of IL-1 and acts upon the substrate Gasdermin family D protein (GSDMD). This evidence concerns the gene CASP3 and infection.