Although women characterized by any of the three definitions of malaria infection tended to have significantly higher Epo levels than uninfected women (maternal: Table 3; placental: NS; any: p = 0.004), none of the proxies for foetal hypoxia examined in the study (cord Epo, placental and cord cortisol, and placental CRH) were increased in the neonates of malaria-infected women (Tables 3 and 4). This evidence concerns the gene EPO and malaria.