Most data support the idea that patients with hot or inflamed tumors, which harbor markers of preexisting functional antitumor T-cell immunity [e.g., interferon (IFN)-γ signaling, high PD-L1 expression, high prevalence of tumor-infiltrating lymphocytes (TILs), or genomic instability], tend to respond relatively well to PD-1/PD-L1 inhibition (12, 41, 42). Here, CD274 is linked to neoplasm.