Although EGFR signaling can be pro-inflammatory in some contexts, astrocyte-specific deletion of Egfr during an immune-mediated murine model of MS led to increased activation of NFκB and downstream expression of target genes, demonstrating that astrocyte-specific EGFR signaling functions to dampen neuroinflammation [44]. The gene discussed is NFKB1; the disease is myeloid sarcoma.