Mechanistically, early infection transiently activated NRF2 via AKT-dependent inhibition of GSK3β, enhancing antioxidant defenses, but prolonged infection suppressed NRF2 activity due to AKT dephosphorylation and GSK3β activation, sustaining NOX4 upregulation and exacerbating oxidative stress. The gene discussed is GSK3B; the disease is infection.