A compelling body evidence supports a causal role for lipoprotein(a) in atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve stenosis (CAVS) as demonstrated by large epidemiological,13 genome-wide association4 and Mendelian randomisation studies.5 As a result, therapeutic strategies to lower Lp(a) (using injectable therapies based on antisense oligonucleotides14 and small interfering RNA molecules,15 followed recently by an orally active therapy16) have progressed rapidly with publication of clinical outcomes studies anticipated in the next 3–5 years. This evidence concerns the gene LPA and atherosclerosis.