Interestingly, the study of TP53-mutated AMLs, a subgroup associated with a very poor outcome, showed that these leukemias are characterized by a higher expression of IFN-γ, FOXP3, immune checkpoints, and markers of immune senescence; seven out of 15 patients (47%) with refractory/relapsed AML and TP53 abnormalities achieved a complete response following immunotherapy with flotetuzumab [90]. The gene discussed is IFNG; the disease is acute myeloid leukemia.