Collectively, our EAE modeling data, together with observations on the association between HCY and MS brain atrophy, suggest that diminished 1,25(OH)2D3-VDR signaling in CD4+ T cells, neurons, or glial cells might decrease BHMT1 activity, reduce SAM availability, increase HCY, and ultimately cause neuronal cell toxicity. The gene discussed is CD4; the disease is myeloid sarcoma.