Since systemic B4galt5-deficient mice are embryonically lethal due to placental dysplasia or hematopoietic failure33–35, the generation of proximal tubule–specific B4galt5-deficient mice will help elucidate the pathogenic role of GlcCer accumulation in the AKI-to-CKD transition. This evidence concerns the gene B4GALT5 and chronic kidney disease.