In the valves, we showed that reduced function of Sox9 during mid-stages of valvulogenesis is sufficient to promote early-onset CAVD in mice [57, 94], and this was mediated, in part, through de-repression of the osteogenic matrix protein Spp1 [93]. The gene discussed is SOX9; the disease is congenital bilateral aplasia of vas deferens from CFTR mutation.