This subset was previously thought to be a contaminant interfering with the suppressive function of Tregs and was neglected previously.[18] However, research by Michel L indicates that this specific population in multiple sclerosis (MS) appears more proliferative and secretes more interferon-γ (IFN-γ) and interleukin-2 (IL-2), both pro-inflammatory cytokines, than healthy individuals [21]. The gene discussed is IFNG; the disease is myeloid sarcoma.