We previously reported that ATM heterozygous mutation in ApoE−/− mice resulted in an overaccumulation of plasma ApoB48-containing lipoproteins and severe hypercholesterolemia occurred only with a combination of a heterozygous ATM mutation and a null ApoE mutation, but not wih the heterozygous ATM mutation alone or with the combined heterozygous ATM and null LDL receptor mutations (7). This evidence concerns the gene APOB and familial hypercholesterolemia.