Together with the clinical data of oxidative stress-related cardiovascular calcification in chronic kidney disease patients [87], these findings indicate that the upregulation of osteoclast-like cell-derived CTSK expression and activity by RANKL/RNAK-p38MAPK or -Erk-1/-2 signaling activation can represent a common mechanism in atherosclerotic plaque calcification (Fig. 2B, middle), implying that CTSK might be a unique molecular target for the management of inflammatory and metabolic ACVD and high-risk calcification. This evidence concerns the gene CTSK and chronic kidney disease.