The article discusses the therapeutic potential of lipoprotein(a) (Lp(a)) inhibitors in the context of cardiovascular disease prevention. Lp(a) has been implicated in the causality of atherosclerosis and calcific aortic stenosis, leading to increased interest in developing novel approaches to integrate Lp(a) into cardiovascular prevention strategies. Current guidelines advocate universal measurement of Lp(a) levels, which can influence cardiovascular risk assessment and triage of high-risk patients for more intensive preventive therapies. Early studies of antisense oligonucleotides, RNA interference, and small molecule inhibitors have demonstrated effective Lp(a) lowering and good tolerability. These agents are moving forward in clinical development to determine their impact on cardiovascular risk. The results of these studies have the potential to transform the approach to cardiovascular disease prevention. Key points include the causal role of Lp(a) in cardiovascular disease, the lack of effective Lp(a) lowering approaches beyond apheresis, and the robust Lp(a) lowering and evaluation of clinical outcomes in novel therapies.The article discusses the therapeutic potential of lipoprotein(a) (Lp(a)) inhibitors in the context of cardiovascular disease prevention. Lp(a) has been implicated in the causality of atherosclerosis and calcific aortic stenosis, leading to increased interest in developing novel approaches to integrate Lp(a) into cardiovascular prevention strategies. Current guidelines advocate universal measurement of Lp(a) levels, which can influence cardiovascular risk assessment and triage of high-risk patients for more intensive preventive therapies. Early studies of antisense oligonucleotides, RNA interference, and small molecule inhibitors have demonstrated effective Lp(a) lowering and good tolerability. These agents are moving forward in clinical development to determine their impact on cardiovascular risk. The results of these studies have the potential to transform the approach to cardiovascular disease prevention. Key points include the causal role of Lp(a) in cardiovascular disease, the lack of effective Lp(a) lowering approaches beyond apheresis, and the robust Lp(a) lowering and evaluation of clinical outcomes in novel therapies.