Besides, stimulation of macrophages with TLR3L in the tumor-bearing mice led to the upregulation of MHCII and costimulatory molecules (e.g., CD80 and CD86), lowered expression of inhibitory molecules (e.g., TIM3), and significant tumor regression in an IFN-αβ signaling-dependent manner [108]. The gene discussed is CD86; the disease is neoplasm.