Recent evidence suggests that the interaction of traditional (i.e., age, smoking, diabetes mellitus [DM], hypertension, and dyslipidemia) and uremia-related so-called cardiovascular risk factors (e.g., hyperphosphatemia, high calcium × phosphorus product, oxidative stress, systemic inflammation, protein energy wasting, P-cresol, fetuin A, the osteoprotegerin (OPG)/receptor activator of NF-κB (RANK)/RANK ligand system, and osteopontin) contributes to excessive and accelerated vascular calcification in CKD patients [5]. Here, TNFRSF11B is linked to hyperphosphatemia.