Also, knockdown of Sox4 inhibited the differentiation of beige adipocytes and reduced the thermogenic capacity and energy metabolism of mature beige adipocytes in vitro. Mechanistically, SOX4 formed a complex with PPARγ and PRDM16, enhanced the binding of PRDM16 to PPARγ, and promoted the transcription of the thermogenic gene Ucp1. These data are of great significance for the development of obesity treatment drugs in the future. This evidence concerns the gene PRDM16 and obesity due to melanocortin 4 receptor deficiency.