Since activation of the myofibroblast phenotype by TGF-β1 is considered a first step towards valvular disease [17], to explore the effect of COX-2 inhibition in CAVD, we induced the calcification of human AVICs isolated from non-calcific aortic valves by 4 days treatment with TGF-β1 [20] in the presence or absence of celecoxib and assessed the number of calcific nodules (CNs). Here, TGFB1 is linked to congenital bilateral aplasia of vas deferens from CFTR mutation.