STAT3 participates in the DNA methylation of tumor suppressor or anti‐apoptotic gene promoters through interaction with DNA (cytosine‐5)‐methyltransferase 1 (DNMT1).[24, 25] Given that acetylation at K685 in the SH2 domain of SHF is crucial for binding of STAT3 to DNMT1, we explored the possibility that SHF could disrupt the interaction of STAT3 and DNMT1. Here, SHF is linked to neoplasm.