A proposed MOA for DMF treatment of MS and psoriasis therefore builds on GSH depletion increasing hemoxygenase-1 expression, impairing STAT1 (signal transducer and activator of transcription 1) phosphorylation, and hereby inhibiting Th1 and Th17 (T helper cell 1 and 17) differentiation6,7. The gene discussed is STAT1; the disease is myeloid sarcoma.