Research by Bai et al. revealed that the mechanism of AraC-induced AML resistance may involve the amplification of TNF-α, which activates the IL-6/STAT3 and NF-KB pathways, enhancing the function and survival of MDSCs and thereby mediating the immune evasion by tumors and drug resistance [165], suggesting that chemotherapy combined with TNF-α-targeting therapy may be an effective strategy to inhibit MDSC-induced immune escape. Here, STAT3 is linked to acute myeloid leukemia.