This is partially explained by i) the heterogeneity of the studied populations, ii) the low presence of subjects with the less common ε2 and ε4 haplotypes, and iii) the confounding impact that plasma lipids have on obesity: body fatness is positively related to circulating cholesterol and triglycerides [7] and, in turn, circulating cholesterol and triglycerides are modulated in a APOE isoform-dependent manner [8]. The gene discussed is APOE; the disease is obesity disorder.