The fetal inflammatory response syndrome plays a central role in the pathogenesis of white matter damage, i.e. cystic periventricular leukomalacia (PVL) in the preterm infant. High levels of proinflammatory cytokines including interleukin-6 (IL-6) have been observed in autopsies of brains of these infants. Thus, an association between IL-6 -174 (G/C) polymorphism, affecting IL-6 transcription rate and plasma cytokine levels, and development of PVL might be hypothesized.We found a significant increased rate of homozygous carriers of the IL-6-174C mutation in mothers with chorioamnionitis and preterm birth with subsequent development of cystic PVL.It could be hypothesized that in pregnant women, who are homozygous carriers of the IL-6-174C mutation, chorioamnionitis could lead to change in the release of the proinflammatory cytokine IL-6. This augmented or secondary up-regulated cytokine could cause a boosted inflammatory response syndrome of the fetus with consecutive damage of the white matter.I hope that this research project might open new horizons and encourage hope for new preventive and therapeutic strategies for the prevention of PVL and cerebral palsy in preterm infants.