Consequently, it has been hypothesized that hesperidin may also act as an immune checkpoint inhibitor in oral cancer cells by targeting PD-L1 expression that has been induced by treatment with IFN-γ via suppression of the STAT1/STAT3 signaling pathway, which ultimately can result in the down-regulation of PD-L1 expression and a decrease in the degree of aggressiveness of cancer cells. The gene discussed is STAT1; the disease is lip and oral cavity carcinoma.