Abstract
The rising incidence of genitourinary (GU) defects among newborns establishes the need and opportunity to focus research efforts on the amelioration of this growing public-health concern. Sadly, our inability to explain the causes of GU defects can be directly attributed to our lack of understanding of GU gene function. Recently, mouse models have been used to provide new insights into the mechanisms that underlie congenital GU malformations.