In progressive MS and long-standing disease patients, white matter plaques were consistently positive for complement proteins (C3, factor B, and C1q), regulators (factor H, C1inh, and clusterin) and activation products [C3b, iC3b, C4d, and terminal complement complex (TCC)] providing evidence that, once established, progression of inflammation in MS may not rely on infiltrating cells but rather on innate immune mechanisms including complement activation (31, 32). The gene discussed is SFXN1; the disease is myeloid sarcoma.