STAT1 and neoplasm: Even though the interplay between the RT-IFN-γ/JAK/STAT1 and IFN-γ/IDO1-p27/STAT1 was unclear yet, we hypothesized that high levels of IDO1 activity at baseline promote tumor outgrowth through immune escape, while the persistent high levels of IDO1 activity during RT resulted in radio-resistance by eliciting tumor-dormancy rather than STAT1-mediated tumor cell apoptosis.