This effect was associated with reduced ROS production, attenuated microglial activation, increased oligodendrocyte progenitor cell proliferation, and increased numbers of mature oligodendrocytes, reaffirming the role of the Hv1 proton channel in controlling NOX-dependent ROS production in the pathogenesis of MS (Liu et al., 2015). The gene discussed is HVCN1; the disease is myeloid sarcoma.