On one hand, it inhibits ovarian cancer proliferation and metastasis by inducing classical pyroptosis via the JAK2/STAT1 pathway; on the other hand, GBP5 reprograms macrophages in the tumor-suppressive microenvironment towards M1 polarization, and its high expression increases the expression of programmed cell death ligand 1 (PD-L1), making it a potential survival marker for tumor patients receiving anti-PD1 and anti-PD-L1 therapy 31. Here, STAT1 is linked to neoplasm.