This in turn caused the production of pro-inflammatory cytokines/chemokines, such as IFN-γ, TNF-α, CXCL9, and CXCL10, and increased interferon regulatory factor 1 (IRF1) and programmed death-ligand 1 (PD-L1) expression, resulting in an enhanced anticancer immune response against primary and lung metastatic B16F10 melanoma compared to untreated controls [113]. The gene discussed is IFNG; the disease is melanoma.