In contrast, the CBA/J × DBA/2J murine model5 spontaneously develops IUGR and embryonic/fetal mortality6, 7 and shares features of the human IUGR complication, including inadequate maternal arterial remodelling at the implantation sites8, 9 and utero-placental dysregulation with complement deposition on trophoblasts, increased inflammatory cell infiltration (neutrophil and monocyte) and tumour necrosis factor (TNF)-α expression in maternal decidua6, 10, 11. The gene discussed is TNF; the disease is fetal growth restriction.