Since the piRNAs from ECpiC#18 are mainly antisense to the STOX1 mRNA, a gene clinically implicated in placental development [51–53], we speculate that mis-regulation of ECpiC#18 might likely impact STOX1 expression and contribute to sperm phenotypes that fall within a hypothesis for paternal factors in the etiology of preeclampsia [74]. This evidence concerns the gene STOX1 and preeclampsia.