The presence of inflammatory cytokines, like interferon γ (IFNγ), interleukin-17 (IL-17) or tumor necrosis factor α (TNFα), but also oncogenes or tumor suppressors can activate the NF-κB-dependent pathway leading to PD-L1 upregulation and maintenance of immune checkpoint blockade [38,52,53,54,55]. The gene discussed is IFNG; the disease is neoplasm.