Collectively, our data demonstrate that (1) in our mouse model of AML, NKp46 deletion results in impaired ILC1 proliferation, reduced production of IFN-γ and TNF by ILC1s, and decreased survival of mice with AML; (2) injection of sufficient Ncr1+/+ ILC1s can prolong the survival of Ncr1gfp/gfp mice with AML. The gene discussed is TNF; the disease is acute myeloid leukemia.