To parse out the specific contribution of OPCs in this process, we established primary cultures of OPCs from WT and TNFR2−/− mice and assessed their response to an inflammatory environment by exposing them to a combination of Th1 cytokines (TNF, IL1β, and IFNγ) known to be highly upregulated in the CNS following EAE and MS (Figure 1A) [27,28]. The gene discussed is IFNG; the disease is myeloid sarcoma.