The inability to prevent pancreatic β-cell loss and to induce regeneration, coupled with the complexity of immune-mediated processes underpinning autoimmune-like changes, has generated the investigation of a wide range of possible pathophysiological processes and factors in T1DM, including the aryl hydrocarbon receptor (AhR) [29], toll-like receptor (TLR)4 activation [30], NF-κB [31], yin yang (YY)1 [32], the melatonergic pathway [33], P53 [18], circadian dysregulation [34], and gut dysbiosis/permeability [35]. The gene discussed is NFKB1; the disease is type 1 diabetes mellitus.