On the other hand, Ferrostatin-1 (Fer-1) treatment promotes the expression of tight junction proteins, implying that inhibition of ferroptosis may act by inhibiting BBB disruption caused by sepsis, acting on a transcription factor called Nrf2, which belongs to a signaling pathway called Nrf-ARE, composed, in addition, of Kelch-like ECH-associated protein 1 (Keap1) and the antioxidant response element (ARE) [36]. The gene discussed is KEAP1; the disease is Sepsis.