In the peripheral blood of untreated patients with psoriasis, the expression levels of inflammasome sensors, IL-1β and IL-18 were enhanced; Verma D et al. demonstrated that TNF-α upregulated pro-IL-1β and pro-IL18 and stimulated these inflammasome activities via increasing ROS and activation of NLRP3 signaling pathways [73]. Here, IL1B is linked to psoriasis.