In Reply First, the purpose of our study 1 was explicitly described as assessing the implications of lipoprotein(a) screening in the context of primary prevention for atherosclerotic cardiovascular disease, with a particular emphasis on individuals not already being treated with statin therapy. Elevated lipoprotein(a) levels for primary prevention includes lifestyle counseling and statin therapy; thus, including individuals already treated with statin therapy may not be informative. 2,3 However, we do agree that, as described in the Limitations section, 1 the UK Biobank cohort has a healthy volunteer bias and is predominately composed of individuals of European ancestry, which may limit the generalizability of some of our results.Second, we do not agree that our statement that extreme lipoprotein(a) levels greater than 200 mg/dL (approximately 500 nmol/L) could have a 3-fold to 4-fold increased risk of atherosclerotic cardiovascular disease is unqualified. Schrock is correct to point out that lipoprotein(a) levels are a continuous variable and display associations with increased risk of atherosclerotic cardiovascular disease at lower levels. Our results, which describe the association between a 120-nmol/L (approximately 50-mg/dL) increase in observed and genetically predicted lipoprotein(a) levels, specifically address this issue. 1 This statement was intentionally made to suggest that, similar to familial hypercholesterolemia, extremely elevated lipoprotein(a) levels can be associated with very high risk of atherosclerotic risk disease but only modestly improve disease discrimination because of its rarity. Accordingly, we state that "efficient strategies to identify individuals with extremely elevated lipoprotein(a) levels require further research." 1 It is also important to note that the cholesterol component of lipoprotein(a) contributes to the total cholesterol measurements used to calculate cardiovascular risk scores using QRISK3 and Pooled Cohort Equations. 4 Thus, these cardiovascular risk scores may underestimate the cardiovascular risk associated with elevated lipoprotein(a) levels when observed or genetically predicted lipoprotein(a) is added to the discrimination models.Third, we agree that identification of elevated lipoprotein(a) levels in an individual patient is indeed helpful for cardiovascular risk assessment. In the Discussion section, 1 we explicitly state approaches such as cascade screening are helpful for identifying families with elevated lipoprotein(a) levels. However, the question that the article sought to address was whether screening for elevated lipoprotein(a) levels in the context of primary prevention for individuals with intermediate cardiovascular risk is useful on a population level, rather than in the context of an individual patient with symptomatic cardiovascular disease. Finally, it is important to mention that the interpretation of these results may change if prospectively demonstrated effective therapies to lower lipoprotein(a) levels become available in the future. 5,6 ...