Elo et al. [28] found a high-level of repression of immune response genes (including MHC Class I and Class II molecules, T-cell receptor signaling, actin filament system and NF-kB signaling) in children that had developed T1D-associated autoantibodies (prediabetes) who eventually progressed to clinical T1D. Here, NFKB1 is linked to prediabetes syndrome.