As we previously showed, this transgenic CaV1.2 expression model increases Ca2+ influx (21) and thereby provides a model that mimics the increased CaV1.2 transcription and protein levels observed specifically in the aortic valves of patients with CAVD (19) and the increased CaV1.2 expression that we detected in a human aortic valve sample (Figure 1A). The gene discussed is CACNA1C; the disease is congenital bilateral aplasia of vas deferens from CFTR mutation.