In light of these findings and our observations that apoC-III was significantly enriched in calcific CAVD tissue, highly present in the disease-prone fibrosa layer, and abundant around calcific nodules, we focused our investigation on whether apoC-III can promote AV calcification as an in vitro proof of concept of the observations we made with our proteomics and immunohistochemistry-generated apolipoprotein CAVD atlas. The gene discussed is APOC3; the disease is congenital bilateral aplasia of vas deferens from CFTR mutation.