A high phosphorylation level of JAK/STAT signaling pathway molecules and transcriptional regulation of STAT3 downstream target molecules were reported in colorectal adenoma, whereas leptin-mediated proliferation and survival were related to the ObRL/STAT3 signaling pathway in colonic tumors; thus, tumor proliferation was inhibited in the case of deficiency of leptin and its receptor, even in severe obesity [50]. This evidence concerns the gene STAT3 and colorectal adenoma.