Despite the insights gained from our study, several limitations should be acknowledged. First, the upstream mechanisms that link PRDX1 ablation in macrophages to the activation of JAK‐STAT1/NF‐κB signaling and M1 polarization remain incompletely defined. Second, our findings regarding the PRDX1‐CUL2‐HIF‐1α axis in cancer cells are primarily based on in vitro evidence, and the in vivo relevance of the PRDX1‐CUL2 interaction warrants further validation. The gene discussed is PRDX1; the disease is cancer.