The canonical NF-κB signaling can be activated by a wide range of stimuli such as ROS, inflammatory cytokines (e.g., tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, and IL-1β), growth factors, radiations, infections, and oncogenic stresses and is in turn responsible for the activation of the NLRP3 inflammasome and the transcriptional induction of pro-inflammatory cytokines (pro-IL-1β and pro-IL-18, converted to mature forms by caspase-1, one of the NLRP3 components) and chemokines (TNF-α) [130]. This evidence concerns the gene IL1B and infection.