Blockade of the renin-angiotensin system (RAS), such as angiotensin-converting enzyme inhibitor and/or angiotensin receptor blocker, has been well appreciated as a renoprotective treatment in proteinuric glomerular diseases. However, not all patients with glomerular diseases respond well to this therapy. Single nucleotide polymorphisms (SNPs) in angiotensin-converting enzyme (ACE) and angiotensinogen may be involved in the inter-individual difference in the responsiveness to the renoprotective efficacy of the RAS blockade. This review focuses on the interface between genomics and therapeutics in the renin-angiotensin system in IgA nephropathy, the most prevalent form of primary glomerulonephritis and one of the major causes of end-stage renal disease in the world.