Consistent with this, lean humans have antibodies to HSP60, presumably arising from other stressors,12 but the level of autoantibodies is increased by obesity that is clearly much more prolonged than in our mice.13 Moreover, we could reverse the hypercholesterolaemic effect of HFD and partially improve glucose tolerance with immunomodulatory HSP60 peptide treatment, implying that autoimmunity to HSP60 contributed to the metabolic disturbances caused by obesity, despite weight not being reduced. This evidence concerns the gene HSPD1 and obesity due to melanocortin 4 receptor deficiency.