IFNG and cancer: The proposed mechanism mediated by elF4A, an essential regulator of STAT1 and therefore PD-L1 expression [40, 43, 44], upon IFN-γ stimulation and increased STAT1 phosphorylation under acidic conditions opens a window for therapeutic interventions to alleviate immune escape of cancer cells by targeting PD-1/PD-L1 signaling.