This paper reviews the evidence that lipoprotein(a) (Lp(a)) is a causal risk factor for cardiovascular disease and discusses current and future management strategies. Genetic studies, particularly Mendelian randomization, have provided strong evidence for the causal relationship between Lp(a) and cardiovascular outcomes. Key genetic variants, such as those in the *LPA* gene, are strongly associated with high Lp(a) concentrations and increased cardiovascular risk. These findings have led to the development of specific Lp(a)-lowering therapies, including mRNA-targeting and small molecule approaches, which are currently in clinical trials. The paper emphasizes the importance of managing traditional risk factors alongside Lp(a) levels to reduce overall cardiovascular risk. Additionally, it discusses the potential of somatic gene-editing therapies for long-lasting Lp(a) reduction. The conclusion highlights the progress made in understanding and treating Lp(a)-associated cardiovascular disease, with ongoing research aiming to translate these findings into clinical practice.This paper reviews the evidence that lipoprotein(a) (Lp(a)) is a causal risk factor for cardiovascular disease and discusses current and future management strategies. Genetic studies, particularly Mendelian randomization, have provided strong evidence for the causal relationship between Lp(a) and cardiovascular outcomes. Key genetic variants, such as those in the *LPA* gene, are strongly associated with high Lp(a) concentrations and increased cardiovascular risk. These findings have led to the development of specific Lp(a)-lowering therapies, including mRNA-targeting and small molecule approaches, which are currently in clinical trials. The paper emphasizes the importance of managing traditional risk factors alongside Lp(a) levels to reduce overall cardiovascular risk. Additionally, it discusses the potential of somatic gene-editing therapies for long-lasting Lp(a) reduction. The conclusion highlights the progress made in understanding and treating Lp(a)-associated cardiovascular disease, with ongoing research aiming to translate these findings into clinical practice.