Figure 2C,D showed that leptin significantly enhanced the DNA-binding activity of STAT3 to the AQP1 promoter, which was suppressed by Rha treatment. This indicates that the leptin-STAT3 axis regulates AQP1 expression and that Rha interferes with this transcriptional regulation. These findings are consistent with previous studies that identified phosphorylated STAT3 as a central regulator of tumor-promoting gene expression in TNBC [43]. This evidence concerns the gene STAT3 and neoplasm.