In the pathogenesis of CAVD, the incomplete understanding of the role of Lp(a) at the molecular level and the absence of appropriate animal models are the current difficulties and dilemmas barriers for the development of specific and effective clinical interventions designed to mitigate the role of Lp(a)—mediated CAVD. The gene discussed is LPA; the disease is congenital bilateral aplasia of vas deferens from CFTR mutation.