Support for this hypothesis is given by results of recent studies showing that calcification in the valve appears largely unrelated to calcifying activity in coronary atherosclerosis [34], and cardiovascular risk factors such as receptor for advanced glycation end products or oxidized low density lipoproteins are implicated in the mechanistic production of reactive oxygen species and bone morphogenetic protein, which promotes valvular interstitial cells activation and leads to osteogenic activity, inflammation, matrix remodeling, fibrosis, and calcification [35]. Here, AGER is linked to coronary atherosclerosis.