Although immunoediting was characterized by the upregulation of the immunosuppressive ligand PD-L1, anti-PD1 therapy had limited efficacy in restoring the anti-leukemia immune response in this model, suggesting that the strategy employed in the immunoedited NrasG12D AML to evade the immune system is likely to be multifaceted. The gene discussed is CD274; the disease is leukemia.