Some chemotherapeutic agents can elicit tumor cell ICD through the release of DMAPs to promote DC maturation, cross‐present tumor‐specific antigens, and prime CD8+ CTL response.[38] However, immune checkpoints such as PD‐L1 are upregulated after chemotherapy or IFN‐γ action,[39] drastically abolishing the functions of CTLs and accelerating T‐cell exhaustion. The gene discussed is IFNG; the disease is neoplasm.