Inhibition of acetyl-STAT3 by SH-I-14 resulted in disruption of STAT3-DNMT1 interaction, de-methylation of TS genes’ promoter regions in triple-negative breast cancer (TNBC) cells in vitro, re-expression of TS genes and inhibition of TNBC tumor growth in vivo. This evidence concerns the gene STAT3 and neoplasm.