The “hot” tumor is often associated with an inflamed immune microenvironment with greater cytotoxic T‐lymphocyte (CTL) infiltration, active interferon (IFN)‐γ status, and sufficient antigen processing and presenting machinery (APM), which were pivotal factors for effective anti‐PD‐1/PD‐L1 therapy.8, 9. The gene discussed is IFNG; the disease is neoplasm.