Advanced glycation end products (AGEs), which are produced in diabetes, bind to the receptor for AGEs (RAGE) to induce NFκB activation, upregulation of RANKL, downregulation of insulin-like growth factor 1 receptor (IGF1R), and increased vascular calcium accumulation.[11–13] Cytokines are increased by activated NFκB and regulate the expression of osteoprotegerin (OPG) and RANKL.[13] Furthermore, RANKL is increased by inflammation, oxidized low-density lipoproteins (oxLDL), AGE, and reactive oxygen species (ROS), which bind to RANK in VSMC membranes causing them to differentiate. Here, TNFRSF11B is linked to diabetes mellitus.