Given the decrease in the osteochondrogenic differentiation observed in the LDLr−/− Runx2ΔSM22, we postulated that Runx2 depletion in myofibroblast-like aVICs and sinus wall cells would block disease progression and ameliorate AS associated with CAVD. Here, RUNX2 is linked to congenital bilateral aplasia of vas deferens from CFTR mutation.