Furthermore, a recent study showed that continuous treatment of melanoma cells with IFN-γ, but not IFN-β, induced radioresistance, through both PD-L1-dependent and -independent mechanisms, and strategic targeting of the JAK-STAT with Ruxolitinib, a JAK1/2 inhibitor, could circumvent the radioresistance [75]. Here, CD274 is linked to melanoma.