As previously reported [59], the mechanistic basis for the hypercholesterolemic effect of NAM HD is due to a delayed clearance of non-HDL lipoproteins that appears to depend strongly on the lack of ApoE, as it has not been observed in wildtype mice (Méndez-Lara et al. unpublished data) treated with a similar NAM dosage. The gene discussed is APOE; the disease is Huntington disease.