APOE and hyperlipidemia: But compared to WHHL rabbits, our founders show robust differences: their LDLR gene mutations are located in the exon 2 and exon 7 and the types of mutations are diverse and, more importantly, it is accompanied by apoE mutations; the WHHL rabbits comprise a deletion in exon 4 of the LDLR gene that encodes a 4-amino-acid deletion in the cysteine-rich ligand-binding domain [32]; their spontaneous hyperlipidemia developed under a normal diet is far more serious than with a high cholesterol diet induced WHHL [35, 36].