Sustained TNF and IFNγ expression produced subpial lesions that extended from the pial surface down to cortical layer III/IV and replicated key pathological characteristics of MS cortical type III lesions, including microglial activation, minimal lymphocytic infiltration and an absence of amoeboid macrophage-like cells [4, 17, 23, 28]. The gene discussed is TNF; the disease is myeloid sarcoma.