This observation, together with increased Ki67, osteopontin, and RUNX2 expression suggest increased proliferation and osteogenic differentiation are occurring in the tissues, which are known hallmarks of CAVD [42] and has been previously reported in various other mouse models [5, 11, 14, 17, 18, 41, 46, 47]. This evidence concerns the gene RUNX2 and congenital bilateral aplasia of vas deferens from CFTR mutation.