Series of experimental, epidemiological, and genetic studies have demonstrated that elevated lipoprotein(a) [Lp(a)] level is associated with cardiovascular disease independently from traditional risk factors of atherosclerosis. This review covers the basics of Lp(a) pathogenicity in atherothrombosis and scrutinizes the biology of proinflammatory activity of the particle. We describe the evidence base around Lp(a) as an independent cardiovascular risk factor by giving an update on the results of epidemiological studies and genetic findings. We have summarized present evidence of Lp(a) lowering strategies and their impact on clinical outcomes in patients with high Lp(a) levels. We highlight a rationale for increased investigational efforts to further assess whether targeting Lp(a) levels minimizes cardiovascular risk.