In fact, tumor inflammation signature, IFN-γ pathway, chemokines, and lymphoid signature scores were higher in TP53-mutated AMLs than in complex karyotype AMLs with WT-TP53; furthermore, expression of immunosuppressive genes, such as FOXP3, IFNG, CD8A, LG3, and GZMB and of immune checkpoints (PD-L1 and TIGIT), is high in TP53-mutated AMLs [89,90]. The gene discussed is FOXP3; the disease is neoplasm.