Several reports suggested that activated VECs might cooperate with activated VICs to promote CAVD progression via the EndMT process; endothelial-derived VICs (eVICs) might further differentiate into osteogenic VICs and contribute to calcification in CAVD, characterized by the up-regulation of osteoblastic markers, such as RUNX2 [6]. This evidence concerns the gene RUNX2 and congenital bilateral aplasia of vas deferens from CFTR mutation.