Consistently, in MDS and AML, decitabine induces higher IFN production34 and improves responses in TP53mut patients.35,36 These observations demonstrated that reprogramming TME was essentially involved in decitabine-treated TP53mut hematological malignancies through fostering IFN production and T cell activation. The gene discussed is IFNA1; the disease is acute myeloid leukemia.