Among the FH cohort, 154 had a heterozygous pathogenic variant in LDLR, APOB, or PCSK9 genes, 63 had high an elevated polygenic score for LDL-C ≥ 90th percentile, 22 had both factors, and 71 had neither, but met the Dutch Lipid Clinics Network criteria for likely or definite FH. Here, LDLR is linked to familial hyperaldosteronism.