This upregulation of the PD-1/PD-L1 axis was shown to contribute to premature death of hematopoietic progenitors in MDS, while hematopoiesis could be recovered by PD-1/PD-L1 blockade in aged S100A9 transgenic mice (which phenotypically resemble MDS) and human MDS bone marrow mononuclear cells [18]. The gene discussed is PDCD1; the disease is myelodysplastic syndrome.