Large epidemiological, Mendelian randomization, and genome-wide association studies have shown that elevated levels of Lp(a) increase the risk of atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve disease (CAVD) (Kamstrup et al., 2008; Clarke et al., 2009; Emerging Risk Factors et al., 2009; Kamstrup et al., 2009; Kamstrup et al., 2014; Burgess et al., 2018; Langsted et al., 2019; Perrot et al., 2019; Trinder et al., 2020a). This evidence concerns the gene LPA and congenital bilateral aplasia of vas deferens from CFTR mutation.