A transgenic mouse line in which NF-κB activation is attenuated specifically in β-cells conferred nearly complete protection against multiple low dose streptozotocin (MLDSTZ)-induced T1D.2 Contrary, mice with constitutively active NF-κB signaling in β-cells spontaneously develop full-blown immune-mediated diabetes.3 Here, NFKB1 is linked to type 1 diabetes mellitus.