In addition, the pharmacological inhibition of caspase-1 with pralnacasan protected from colonic mucosal damage as with NLRP3 deficiency, suggesting that NLRP3 inflammasome contributes to the pathophysiology of intestinal inflammation and that NLRP3 blockade could represent a viable pharmacological strategy for the management of bowel inflammation (39, 40). Here, NLRP3 is linked to inflammation.