Lipoprotein(a) (Lp(a)) is a major genetically determined risk factor for cardiovascular disease (CVD). Recent genetic studies have established a causal relationship between Lp(a) and CVD, showing that higher Lp(a) levels are associated with increased cardiovascular risk. Genetic variants in the LPA gene, such as apo(a) isoform size and kringle IV repeats, strongly influence Lp(a) concentrations and cardiovascular outcomes. These findings have led to the development of specific Lp(a)-lowering therapies currently in clinical trials. Lp(a) concentrations are influenced by genetic factors, with the LPA gene accounting for up to 90% of Lp(a) variance. Variants in the LPA gene, such as rs10455872 and rs3798220, are strongly associated with high Lp(a) levels and increased cardiovascular risk. These genetic variants provide a strong basis for understanding the causal role of Lp(a) in CVD. Current guidelines suggest that Lp(a) concentrations above 50 mg/dL are associated with clinically relevant risk, while those below 30 mg/dL are not. However, the absolute risk depends on other traditional risk factors. Therefore, managing traditional risk factors is crucial for reducing overall cardiovascular risk in individuals with high Lp(a) levels. Lp(a)-lowering therapies, such as mRNA-targeting drugs, are in clinical trials and have shown significant reductions in Lp(a) levels. These therapies, including antisense oligonucleotides (ASOs) and short interfering RNAs (siRNAs), target the production of apo(a) in the liver. Additionally, oral small molecule inhibitors like Muvalaplin are being tested for their ability to inhibit Lp(a) formation. Future developments in Lp(a)-lowering strategies include somatic gene-editing therapies, such as CRISPR/Cas9, which aim to provide long-term and permanent reductions in Lp(a) levels. These advancements could offer new treatment options for individuals with extremely high Lp(a) concentrations. In conclusion, genetic studies have established the causal role of Lp(a) in CVD, leading to the development of specific therapies. These therapies, combined with the management of traditional risk factors, offer new opportunities to reduce cardiovascular risk in individuals with high Lp(a) levels.Lipoprotein(a) (Lp(a)) is a major genetically determined risk factor for cardiovascular disease (CVD). Recent genetic studies have established a causal relationship between Lp(a) and CVD, showing that higher Lp(a) levels are associated with increased cardiovascular risk. Genetic variants in the LPA gene, such as apo(a) isoform size and kringle IV repeats, strongly influence Lp(a) concentrations and cardiovascular outcomes. These findings have led to the development of specific Lp(a)-lowering therapies currently in clinical trials. Lp(a) concentrations are influenced by genetic factors, with the LPA gene accounting for up to 90% of Lp(a) variance. Variants in the LPA gene, such as rs10455872 and rs3798220, are strongly associated with high Lp(a) levels and increased cardiovascular risk. These genetic variants provide a strong basis for understanding the causal role of Lp(a) in CVD. Current guidelines suggest that Lp(a) concentrations above 50 mg/dL are associated with clinically relevant risk, while those below 30 mg/dL are not. However, the absolute risk depends on other traditional risk factors. Therefore, managing traditional risk factors is crucial for reducing overall cardiovascular risk in individuals with high Lp(a) levels. Lp(a)-lowering therapies, such as mRNA-targeting drugs, are in clinical trials and have shown significant reductions in Lp(a) levels. These therapies, including antisense oligonucleotides (ASOs) and short interfering RNAs (siRNAs), target the production of apo(a) in the liver. Additionally, oral small molecule inhibitors like Muvalaplin are being tested for their ability to inhibit Lp(a) formation. Future developments in Lp(a)-lowering strategies include somatic gene-editing therapies, such as CRISPR/Cas9, which aim to provide long-term and permanent reductions in Lp(a) levels. These advancements could offer new treatment options for individuals with extremely high Lp(a) concentrations. In conclusion, genetic studies have established the causal role of Lp(a) in CVD, leading to the development of specific therapies. These therapies, combined with the management of traditional risk factors, offer new opportunities to reduce cardiovascular risk in individuals with high Lp(a) levels.