Identifying the appropriate treatment for PPROM requires good knowledge of the mechanisms that lead to amniochorionic membrane rupture, in labor or prematurely, whether they are genetic in nature (apoptosis of the amniotic epithelium and chorionic trophoblast), epigenetic (changes in the structure of MMP and TIMP promoter genes), physical (excessive stretching membranes), inflammatory (cytokines released by immune cells lead to high levels of oxidative stress), or hormonal (increased levels of relaxin). This evidence concerns the gene TIMP1 and preterm premature rupture of the membranes.