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Furthermore, it has been demonstrated that the IFN–STAT1 pathway functions as an effector of DDR components in cancer cells by inhibiting flap endonuclease-1 (FEN1), which affects human leukocyte antigen (HLA-DR) and programmed death receptor ligand 1 (PD-L1) to suppress the tumorigenesis dependent on the IFN-γ–JAK–STAT1 pathway in oral squamous cell carcinoma [221]

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1 ) caused by increased levels of interleukin (IL)-6 and tumor necrosis factor α (TNF-α) along with decreased levels of interferon α and interferon β (IFN-α, IFN-β) [6]