Combining this information, along with our recent data showing that APOE promotes diet-induced obesity independent of its ability to mediate direct peripheral post-prandial lipid delivery to WAT[57], an alternative interpretation of the data of Hofmann et al. [54] is that the obesity resistant phenotype of floxed-lrp1 mice crossed with aP2-cre mice is due to Lrp1 inactivation in PNS and CNS and not in adipose tissue, as originally suggested[54]. The gene discussed is APOE; the disease is Obesity.