To dissect the mechanisms of GEC injury in early DKD in an unbiased way, we previously conducted a transcriptomic analysis of sorted GECs from diabetic mice lacking endothelial nitric oxide synthase,[5] as well as single‐cell transcriptomic analysis of glomerular cells from the same mouse model.[6] These studies identified several important genes that are highly regulated in GECs in early DKD, among which were Lrg1,[7]Gpr56,[7, 8] and Ch25h. The gene discussed is CH25H; the disease is diabetic kidney disease.