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. This evidence concerns the gene PPARG and obesity disorder.