Irrespective of whether genetic polymorphism in ARHGEF11 or other Rho-ROCK genes are ultimately causative to CKD, pharmacological inhibition of this pathway via ROCK (fasudil and Y-27632) has been demonstrated to be effective at improving proteinuria, glomerulosclerosis, and fibrosis in experimental animal models [34–36]. This evidence concerns the gene ARHGEF11 and chronic kidney disease.