In asthma, airway epithelia convert thiocyanate and H2O2 into hypothiocyanite (OSCN−) via the pendrin/dual oxidase/peroxidase axis; low OSCN− doses activate NF-κB via protein kinase A to induce chemokines, while high levels trigger necrosis and IL-33 release, amplifying type-2 inflammation—a pathway attenuated by heme peroxidase inhibitors (antithyroid agents) [138]. The gene discussed is NFKB1; the disease is asthma.