Furthermore, because the signaling pathway by which IL-1a drives PD-L1 expression is non-overlapping with IFN-g and IL-27, our findings suggest that genetic defects in tumor cell STAT1 signaling, which can be acquired under the selection pressure of anti-PD-1 therapy [23], would not interfere with the ability of IL-1a to sustain tumor cell expression of PD-L1. Here, CD274 is linked to neoplasm.