The blockade of PD-1, PD-L1, or TIM-3 resulted in the upregulation of various genes related to the activation of the IFN-γ signaling pathway; some of them encode inflammatory cytokines (such as IFN-γ, TNF-α, and GM-CSF), transcription factors (such as T-bet) and key signaling mediators (such as STAT1 and STAT4) involved in the maintenance and differentiation of the Th1 immune response, which plays a key role in anti-tumor immunity, and the recruitment and activation of effector immune cells, such as M1 macrophages, dendritic cells and natural killer (NK) cells [45,46,50]. The gene discussed is CSF2; the disease is neoplasm.