CH25H and diabetic kidney disease: The vascular endothelial cell dysfunction in DKD is multifaceted.  Altered nitrogen oxide (NO) production, reactive oxygen species production, and lipid metabolism are involved in endothelial cell injury in DKD.[23] It is known that GECs undergo neo‐angiogenesis at the early stage but their apoptosis increases in parallel leading to decreased GECs in progressive DKD.[5] We found that CH25H loss caused significant kidney endothelial cell apoptosis in diabetic mice, which may underlie the more severe DKD phenotype in the diabetic Ch25h‐null mice.