Indeed, we detected glia-specific hypermethylation of the HBEGF promoter in patients with MS compared with non-neurological controls in proximity to HIF1α binding sites, suggesting that the epigenetic suppression of trophic HB-EGF signaling may be of particular relevance in glial cells during progressive stages of MS (Fig. 8b, Extended Data Fig. 9b and Supplementary Table 5). The gene discussed is EGF; the disease is myeloid sarcoma.