In non-obese diabetic (NOD) mice (T1DM model) or streptozocin (STZ) induced T1DM model mice, β-cell-specific overexpression of Trx1 markedly reduces the incidence of diabetes without improving insulin secretory capacity, insulin content, or the development of insulitis compared with those of littermate controls (55). The gene discussed is INS; the disease is type 1 diabetes mellitus.