Qiang and co-authors uncovered that Prdm16 specifically interacts with deacetylated Pparγ, which is mediated by SIRT1 (on Lys268 and Lys293), and that SIRT1 gain-of-function resulted in the upregulation of BAT-selective gene expression (Ucp1) and the downregulation of WAT-selective gene expression involved in insulin resistance (Agt, Chemerin, Pank3, Resistin, and Wdnm1L) in vitro (127) (Figure 7B). The gene discussed is SIRT1; the disease is Insulin resistance.