2024) that the minor allele frequency (MAF) of this variant in the non‐FH subjects in the 100,000 genome (general population) sample was 8 × 10−5 (12 out of 77,275 individuals), with a highly significant enrichment of this variant in a sample of those individuals with clinical FH (10 out of 467 individuals, MAF = 0.01). Based on this work, we estimate that ∼2% of individuals in the United Kingdom with a clinical diagnosis of FH have this APOE variant as their monogenic cause. Here, APOE is linked to familial hyperaldosteronism.