To be specific, IFN-γ could induce the expressions of multiple immune checkpoints including cytotoxic T lymphocyte antigen-4 (CTLA-4), PD-L1, and PD-L1 via JAK-STAT-dependent transcriptional cascade.349–351 The facilitation of PD-L1 by IFN-γ in melanoma cells is highly related to p53 expression.350 These data indicate that IFN-γ might modulate tumoral immune checkpoint to terminate the immune surveillance of tumor cell performed by lymphocytes, namely, immune evasion. The gene discussed is IFNG; the disease is melanoma.