Furthermore, studies using either POMC or ObRb-expressed neuron-specific SOCS3 transgenic mice indicated that SOCS3 upregulation alone in proopiomelanocortin (POMC) neurons, but not in ObRb neurons, is sufficient to cause leptin resistance and obesity, mediated by the antagonization of phosphorylated STAT3 and mTOR-S6K signaling due to SOCS3 upregulation [41]. This evidence concerns the gene STAT3 and obesity due to melanocortin 4 receptor deficiency.