In the US alone, more than 20 million people suffer from kidney disease. Despite the significant burden of renal disease for the individual and society, treatment options are limited. Over the years, the identification of genes and molecular pathways required for normal renal development has provided insight into our understanding of obvious developmental diseases such as renal agenesis and renal dysplasia. However, many of the genes identified have also been shown to play roles in adult-onset and acquired renal diseases such as focal segmental glomerulosclerosis (scarring of the renal filters). In fact, data suggest that the number of glomeruli and nephrons (filtering units) present in the kidney at birth, which is determined during fetal life, predicts the risk of kidney disease and hypertension later in life; a reduced number is associated with greater risk. To discover novel therapeutic targets and strategies to slow and reverse kidney disease, we must continue to dissect the molecular mechanisms that underlie kidney development.