Building upon a study showing an association between increased expression of CaV1.2 in the aortic valve and CAVD (19), our combination of VIC culture and in vivo models demonstrates that increased Ca2+ influx through CaV1.2 is, indeed, causal for the initiation of calcific lesions within the aortic valve. The gene discussed is CACNA1C; the disease is congenital bilateral aplasia of vas deferens from CFTR mutation.