Specifically, obesity-associated enhancements in Treg abundance, activation, and markers of both functional potency and phenotypic stability in the murine airway were associated with alterations in the biosynthetic commitment of acetyl-CoA to general and Treg-specific processes (i.e., acetylation of polyamines for export and the post-translational modification FoxP3). The gene discussed is FOXP3; the disease is obesity due to melanocortin 4 receptor deficiency.