Profound immunosuppression mediated by myeloid-derived suppressor cells, the upregulation of cytokines and cell-surface receptors on leukemic cells, the suppression of native immune regulator cells, and metabolic aberrations in the bone marrow are features of the <i>TP53</i>-mutated AML/MDS marrow microenvironment. This evidence concerns the gene CD177 and myelodysplastic syndrome.