Intriguingly, it’s been verified that after treating MDSCs with interleukin (IL)-6 in the vitro tumor-bearing mice model, the activation of STAT3 further elevated expression of DNMT1 and DNMT3B, resulting in the decreased downstream signaling pathway such as tumor necrosis factor-α (TNF-α)-induced and receptor interacting serine/threonine kinase 1 (RIP1)-dependent necroptosis, eventually promoting MDSCs survival and accumulation [99]. Here, DNMT1 is linked to neoplasm.