AIDs are also considered to be interleukin (IL)-1-mediated diseases that respond to anti-IL-1 therapies; in fact, autoinflammation is characterized by an overactivation of the innate immune system and by the overproduction of proinflammatory cytokines including IL-1β, IL-18, tumor necrosis factor (TNF), and type-1 interferons (IFNs) [9,10,11]. This evidence concerns the gene IL1B and AIDS.