NOD mice unable to produce NADPH oxidase (NOX)-derived superoxide (Ncf1(m1J)) are protected against T1D development, and present an impaired M1 pro-inflammatory activation of islet macrophages with a concomitant increase in M2 polarisation, as indicated by chemokine levels in the sera and the surface markers detected upon islet staining [85]. The gene discussed is NCF1; the disease is type 1 diabetes mellitus.