Since resident microglial activation and macrophage infiltration into the CNS are common features of both MS and EAE, initial interest in the role of KP metabolism in the pathogenesis of EAE arose from findings that cultured human macrophages can produce QUIN at neurotoxic levels in response to acute treatment with IFN-γ (Heyes et al., 1992; Chiarugi et al., 2001a). This evidence concerns the gene IFNG and myeloid sarcoma.