Nevertheless, the currently available evidence indicates that, in T2D-associated target organ damage, innate immune receptors and inflammasomes, notably including the inflammasome NLRP3, and increased production of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 [11,14], play a role here. The gene discussed is TNF; the disease is type 2 diabetes mellitus.