As an alternative, we have developed an IFNα mimetic from its C-terminal, denoted as IFNα-C that offers two distinct advantages: 1) In a mouse model of MS, IFNα-C protected mice against the remitting/relapsing episodes of paralysis, without the attendant toxicity seen in the parent IFN [30]; 2) Since receptors for type I IFN are ubiquitous, therapeutic IFN is often “soaked up” by the unwanted cells and tissues before reaching its target organ, which may explain why a higher dose is required to attain therapeutic efficacy. The gene discussed is IFNA2; the disease is myeloid sarcoma.