The authors proposed that, in the mentioned tumors, STAT3 interacted with DNA methyltransferase 1 (DNMT1) and the STAT3-DNMT1 complex catalyzed the methylation and consequent inactivation of some tumor-suppressor genes such as p53 and PTPN6. Interestingly, the STAT3 K685R mutation reduced tumor growth through interruption of the STAT3–DNMT1 interaction and consequent reactivation of a set of tumor-suppressor genes. This evidence concerns the gene TP53 and neoplasm.