The purpose of this article is to review the current state of the art on 2 newly postulated drivers of uremic cardiomyopathy, elevated circulating fibroblast growth factor‐23 (FGF23) and reduced αKlotho, and discuss how recent insights into the pathophysiological processes has led to development of potential therapeutic options aimed at reducing the cardiovascular risk of patients with CKD/ESRD. The gene discussed is FGF23; the disease is chronic kidney disease.