Interestingly, when MS patients were given GA or IFN-β, the defective immunoregulation of TIM-3 was reversed, and the increase in IFN-γ production of CD4+ T cells in both groups of control and MS patients was comparable, suggesting that TIM-3 regulation is a therapeutic mechanism of these drugs [122]. The gene discussed is HAVCR2; the disease is myeloid sarcoma.