Despite the association between advanced age and consumption of HFD, conditions that are already known to favor the onset of metabolic diseases [48], the deletion of ACE2 at the age of 12 months did not change BW, fat deposition, or plasma lipid and glucose homeostasis, demonstrating a delayed effect of HFD in ACE2-/y mice, suggesting that ACE2 in an old age no longer interferes with these parameters as observed at younger ages, and that the mechanism of protection against HFD-induced obesity could be age-dependent. The gene discussed is ACE2; the disease is obesity disorder.