They suggested a hypothetical model in which suppression of macrophage IL-12p35 and IL-12p40 signaling by IL-2 in the macrophage-competent HSV-IL-2 infected mice, and the lack of IL-12p70 due to macrophage depletion play a key role in the CNS demyelination in these models of MS. The gene discussed is IL2; the disease is myeloid sarcoma.