In particular, inhibiting the conversion of cytochrome c–Fe3+ to cytochrome c–Fe2+ reduced inflammation in models of T cell–mediated disease, such as intestinal inflammation, EAE, psoriasis, and T cell–driven asthma (6), indicating that the ferrous (Fe2+) form of iron is essential to T cell effector function. The gene discussed is CYCS; the disease is psoriasis.