2023), can combine to elevate LDL‐C concentrations to those seen in monogenic FH. While individuals with this ‘polygenic hypercholesterolaemia’ do have an elevated CHD risk, this is lower than in those with monogenic FH, and risk can be lowered more successfully by LLT. The FH phenotype can also be mimicked by having a combination of SNPs at the LPA locus, which results in high concentrations of the LDL‐C‐related particle Lp(a). This evidence concerns the gene LPA and familial hyperaldosteronism.