Specifically, during the early phase of infection, Brucella activates the GTP cyclohydrolase 1 (GCH1)-tetrahydrobiopterin (BH4) axis, a GPX4-independent antioxidant mechanism that suppresses lipid peroxidation and ferroptotic cell death in macrophages, thereby creating a permissive niche for bacterial replication. Here, GCH1 is linked to infection.