Moreover, besides pharmacological inhibition of MAPK, one could speculate that selective depletion of specific AP-1 components (e.g., via siRNA or crisp genetic ablation or novel small molecules) could remove the inhibitory braking exerted by co-inhibitory checkpoints (e.g., PD-1/PD-L1) or impair the immunosuppressive Tregs and thus restore the effective anti-tumor T-cell responses and synergistically augment the efficacy of immunotherapy. Here, PDCD1 is linked to neoplasm.