In addition to regulation of GSH production, we also found that BLP‐trained macrophages augmented their antioxidative capability by upregulating several key antioxidant molecules such as SOD2, CAT, GSTA3, and PRDX6[69] In particular, the transcription factor NRF2 pathway, which plays an important regulatory role in resisting the oxidative stress response,[40] was significantly more activated in BLP‐trained macrophages than in naïve macrophages, while knocking out NRF2, the ability of BLP‐trained macrophages to resist ferroptosis upon bacterial infection was markedly impaired. The gene discussed is GSTA3; the disease is bacterial infectious disease.