Excessive IL-1β production in T2DM has a few consequences: (1) it induces the expression of other inflammatory mediators (IL-18, IL-33) using IL-1 receptor signaling that amplifies inflammatory reaction [183]; (2) it evokes oxidative stress as well as ER stress, which are both closely linked to T2DM [184,185]; and (3) it activates c-Jun N-terminal kinases (JNKs), inducing serine phosphorylation of insulin receptor substrate 1 (IRS-1) and attenuating the activity of the insulin-PI3K/AKT signaling pathway in insulin-sensitive tissues [186]. This evidence concerns the gene IL18 and type 2 diabetes mellitus.