Fetal growth restriction (FGR) is a common clinical problem that has a significant effect on perinatal morbidity and mortality. In addition, it also adversely influences adult health, as it increases the risk of cardiovascular disease and impaired glucose tolerance. There is growing evidence that genes play a role in the pathogenesis. Karyotypic abnormalities, affecting both the fetus and the placenta, are known to be associated with fetal growth restriction. This not only impacts on clinical management but has also aided the understanding of the mechanisms controlling fetal growth. In particular, there is an increasing appreciation of the role of imprinted genes in growth and development. There is good genetic epidemiological evidence that genes also play a role in the more common, multifactorial fetal growth restriction, seen in the presence of a normal karyotype. The number of candidate genes studies is increasing and includes members of the renin angiotensin system and the insulin-like growth factor axis. The most extensively investigated to date are the inherited thrombophilias and meta-analyses seem to support an association with fetal growth restriction. However, larger studies are urgently required to confirm this association. There is currently no evidence to support screening low-risk pregnant women for inherited thrombophilias, and there are no randomised controlled trials to suggest that treatment with anticoagulants improve outcome. At present screening or treatment should occur only within such trials.