PURPOSE OF REVIEW: Lipoprotein(a) has been identified as a causal risk factor for atherosclerotic cardiovascular disease (ASCVD) and aortic valve stenosis. However, as reviewed here, there is ongoing debate as to the key pathogenic features of Lp(a) particles and the degree of Lp(a) atherogenicity relative to low-density lipoprotein (LDL). RECENT FINDINGS: Genetic analyses have revealed that Lp(a) on a per-particle basis is markedly (about six-fold) more atherogenic than LDL. Oxidized phospholipids carried on Lp(a) have been found to have substantial pro-inflammatory properties triggering pathways that may contribute to atherogenesis. Whether the strength of association of Lp(a) with ASCVD risk is dependent on inflammatory status is a matter of current debate and is critical to implementing intervention strategies. Contradictory reports continue to appear, but most recent studies in large cohorts indicate that the relationship of Lp(a) to risk is independent of C-reactive protein level. SUMMARY: Lp(a) is a highly atherogenic lipoprotein and a viable target for intervention in a significant proportion of the general population. Better understanding the basis of its enhanced atherogenicity is important for risk assessment and interpreting intervention trials.