AML blasts also evade immune attack through immune editing, a mechanism by which AML cells function like myeloid-derived suppressor cells by secreting arginase-1, indoleamine 2–3 dioxygenase, and inducible nitric oxide synthetase, which suppress T-cell function by inducing anergy, cell cycle arrest, and programmed cell death [50]. The gene discussed is ARG1; the disease is acute myeloid leukemia.