Certain changes in cellular function are characteristic of renal disease. Foremost among these is the excessive proliferation of cells, but other phenotypic changes include dysregulated apoptosis, migration, adhesion, contraction, secretion, and receptor expression. Recent advances in cell biology have revealed an extensive role for the small monomeric GTPases of the Ras superfamily in the control of these cellular events through intracellular signalling cascades. The specific Ras genes appear to play discrete and identifiable roles in a range of complex signalling networks. These insights lead to the possibility of targeting Ras genes in a specific manner in renal therapies. For example, the process of renal cell proliferation might be sensitive to downregulation of Harvey Ras and Kirsten Ras; targeting of Rho A and related species may modulate cell migration, fibrosis, and intrarenal vasoconstriction. Possible strategies for such modulation could include the use of RNA-interacting agents such as antisense DNA and si-RNA and the use of small molecules acting on Ras directly or on related signalling molecules such as Rho kinase and Raf kinase.