Controlling the development of vascular calcification in chronic kidney disease is essential, because it is associated with increased cardiovascular pathology. However, the precise mechanism of vascular calcification has not been completely elucidated. In the literature, the involvement of passive calcium and phosphate deposition as well as an active process stimulating the transformation of vascular smooth muscle cells into an osteoblastic phenotype is suggested. New promising insights into the etiology could lead to better treatment strategies, as Mizobuchi et al. now report.