TCF7L2 and Infertility: If these genes play roles in placental development, there is evidence for redundancy as TCF7L2 knockout mice lack a placental phenotype and are developmentally normal at birth, and murine and human GDF15 knockouts are reportedly normal and fertile.6,57–59 Conversely, IGFBP7 and PGR were primarily found in maternally derived spiral arteries, suggesting a maternal genetic contribution to spiral artery remodeling, and knockout of these genes in murine models contributes to a reduction in litter size and infertility, respectively.60,61