Specifically, high doses (5–10 μg/day) of IFN-γ exhibited an anti-AML effect, whereas low doses (0.01–0.05 μg/day) accelerated AML development and promoted the self-renewal of LSCs in patient-derived AML-LSCs as well as in a mouse model enriched for LSCs driven by MLL-AF9 [99]. The gene discussed is MLLT3; the disease is acute myeloid leukemia.