Previously, we demonstrated that mice lacking the endothelial glucocorticoid receptor (GRECKO) were highly susceptible to streptozotocin-induced diabetic nephropathy and demonstrated augmented Wnt signaling, aberrant cytokine reprogramming, and suppressed fatty acid oxidation (FAO) (5, 6), leading to the conclusion that the endothelial glucocorticoid receptor (GR) is a key regulatory molecule in the pathophysiology of renal fibrosis. The gene discussed is NR3C1; the disease is renal fibrosis.