Thyroid thermogenesis phenomenon has been well known for more than one century. However, how thyroid hormones stimulate thermogenesis remains largely unclear. In the present study we show that fat Klf9 expression is markedly induced by T3. Moreover, Klf9 expression level in human WAT is inversely correlated to adiposity. Klf9 overexpression in primary fat cells stimulates cellular thermogenesis, which is UCP1-dependent. Fat-specific Klf9 transgenic mice gain less weight and have smaller fat pads due to increased thermogenesis of brown and beige fat. Klf9 transgene markedly promotes browning of white adipose tissue. Conversely, Klf9 mutation in brown adipocytes reduces expression of thermogenic genes, causing a reduction in cellular respiration. Global Klf9 mutant mice exhibited obesity and cold sensitivity due to the impaired thermogenic function of fat. Furthermore, fat-specific Klf9-deleted mice are prone to obesity on a high-fat diet. Finally, fat Klf9 deletion inhibits the T3-mediated induction of browning of WAT and thermogenesis of BAT. Mechanistically, T3/TRα complex directly bind to Klf9 gene promoter and activate its expression in fat, which in turn stimulates PGC1α, a master regulator of fat thermogenesis, subsequently promoting energy expenditure. The present study reveals a critical role for Klf9 in mediating thyroid thermogenesis. Targeting Klf9 in fat might be therapeutically exploited to treat obesity and metabolic diseases, while avoiding the side effects of thyroid hormones.