PPARα/γ agonism in the liver is known to be metabolically beneficial, however, previous literature reporting knockout of PPARγ in macrophages or in vivo treatment with a PPARγ agonist suggests that PPARα/γ agonism in macrophages (including Kupffer cells in the liver) might be sufficient to reduce obesity-associated dysmetabolism 26, 27. Here, PPARG is linked to obesity due to melanocortin 4 receptor deficiency.