Furthermore, although the JAK-STAT3 pathway may maintain the phenotype and function of tumor stem cells by regulating anabolic and catabolic metabolism, the exact pathway by which this is achieved remains unclear.26 Recently, it has been shown that human adipocyte-derived leptin, via activation of JAK-STAT3 signaling, promotes STAT3 phosphorylation and entry of p-STAT3 into the nucleus to bind to the carnitine palmitoyltransferase 1 B (CPT1B) promoter. This evidence concerns the gene CPT1B and neoplasm.