The activation of NF-κB leads to the transcription of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β), which in turn can further activate NF-κB, intensifying the inflammatory response and hastening the progression of diabetes. This evidence concerns the gene IL6 and diabetes mellitus.