Data supporting the key role for immune mechanisms in PR (47) show significantly lower concentrations of interferon-γ in remitters compared to non-remitters and controls, a higher frequency of CD4+ CD25+-CD127hi cells, and a non-Treg subset of memory T cell, which are all consistent with a slower rate of progression of T1D (48, 49). The gene discussed is CD4; the disease is type 1 diabetes mellitus.