There is clinical proof-of-concept that pro-inflammatory cytokines, such as interleukin 1β (IL-1β) or tumour necrosis factor α (TNFα), released by macrophages, dendritic cells, and even β-cells themselves during pancreatic islet inflammation, contribute to the loss of pancreatic β-cell function in both type 1 diabetes (T1D) and type 2 diabetes (T2D) [2,3]. This evidence concerns the gene TNF and type 1 diabetes mellitus.