We recently reported that endothelial dysfunction in the aortic valve increases DPP-4 expression, thereby leading to induced degradation of insulin-like growth factor-1 (IGF-1) and the subsequent osteogenic differentiation of VICs, and that sitagliptin, a selective DPP-4 inhibitor that has been broadly used for the treatment of human type 2 diabetes mellitus, hindered the progression of aortic valve calcification in CAVD animal models [19]. The gene discussed is DPP4; the disease is aortic valve calcification.