We addressed this limitation by using two different approaches: 1) Immune-competent mouse syngeneic tumor models: high doses of DN052 were used to offset the low TLR8 activity in rodents; 2) Human AML mouse xenograft model: human HL-60 AML cells could be directly targeted by TLR8 agonist through its effect of inducing terminal differentiation-mediated tumor suppression [24]. The gene discussed is TLR8; the disease is neoplasm.