Inflammasomes activation is critical for both innate and adaptive immunity through their regulation of interleukin 1?茁(IL-1?茁) and IL-18. Prolonged inflammasomes activation can lead to exaggerated expression of signaling components as well as pro-inflammatory cytokines that can damage the host, resulting in chronic inflammatory diseases and autoimmune disorders. Therefore, pathways of deactivation are important to balance the immune responses. However, recent discoveries have uncovered a plethora of pathogenic strategies to inhibit the activation of inflammasome signal pathways and the production of pro-inflammatory cytokines to evade immune responses. Elucidation of these mechanisms might be helpful to the rational design of therapy against infectious diseases and other inflammasome-dependent inflammatory processes.