An ongoing project aims to correctly label such sequence variants as non-pathogenic.[24] A final possible explanation is that other genetic variants counterbalanced the effect of the FH mutation, such as concurrent ApoB or loss-of-function PCSK9 mutations that usually result in hypobetalipoproteinemia.[25]–[27] We aim to perform additional studies in the near future to find out whether the proposed putative explanations hold true. The gene discussed is APOB; the disease is hypobetalipoproteinemia.