Because hypoxia-induced activation of NF-κB activity in cells results in transcriptional activation of genes that encode for the proinflammatory cytokines (such as IL-1β) [14, 17, 22] and epithelial cells are exposed to chronic or cycling hypoxia in prostate tumors [19, 21], we investigated whether hypoxia could activate the NF-κB activity and “prime” PrECs for activation of the NLRP3 or AIM2 inflammasome activity. This evidence concerns the gene IL1B and prostate neoplasm.