Lipoprotein(a) [Lp(a)] plays a causal role in cardiovascular disease and is a significant risk factor for atherosclerosis and calcific aortic stenosis. Current guidelines recommend measuring Lp(a) levels to assess cardiovascular risk and guide treatment. Despite the lack of effective therapies to lower Lp(a) levels, recent advances have led to the development of novel therapeutics, including antisense oligonucleotides, RNA interference agents, and small molecule inhibitors, which can significantly reduce Lp(a) levels. These agents are being evaluated for their clinical outcomes and potential to reduce cardiovascular risk. Early studies show that these therapies are well-tolerated and effective in lowering Lp(a) levels. However, the field lacks therapies that selectively and robustly reduce Lp(a) levels. Ongoing clinical trials are assessing the impact of these therapies on cardiovascular events, with the potential to transform cardiovascular disease prevention. The results of these trials will determine whether Lp(a) lowering can effectively reduce cardiovascular risk. Current research also highlights the importance of Lp(a) in aortic valve disease and its association with calcific aortic stenosis. The development of gene-editing approaches, such as CRISPR/Cas9, is also being explored for Lp(a) reduction. While these therapies show promise, their long-term safety and efficacy need to be evaluated in large clinical trials. The potential of Lp(a) lowering to reclassify cardiovascular risk and improve patient outcomes remains a key focus of ongoing research.Lipoprotein(a) [Lp(a)] plays a causal role in cardiovascular disease and is a significant risk factor for atherosclerosis and calcific aortic stenosis. Current guidelines recommend measuring Lp(a) levels to assess cardiovascular risk and guide treatment. Despite the lack of effective therapies to lower Lp(a) levels, recent advances have led to the development of novel therapeutics, including antisense oligonucleotides, RNA interference agents, and small molecule inhibitors, which can significantly reduce Lp(a) levels. These agents are being evaluated for their clinical outcomes and potential to reduce cardiovascular risk. Early studies show that these therapies are well-tolerated and effective in lowering Lp(a) levels. However, the field lacks therapies that selectively and robustly reduce Lp(a) levels. Ongoing clinical trials are assessing the impact of these therapies on cardiovascular events, with the potential to transform cardiovascular disease prevention. The results of these trials will determine whether Lp(a) lowering can effectively reduce cardiovascular risk. Current research also highlights the importance of Lp(a) in aortic valve disease and its association with calcific aortic stenosis. The development of gene-editing approaches, such as CRISPR/Cas9, is also being explored for Lp(a) reduction. While these therapies show promise, their long-term safety and efficacy need to be evaluated in large clinical trials. The potential of Lp(a) lowering to reclassify cardiovascular risk and improve patient outcomes remains a key focus of ongoing research.