The notion that neutrophils play a pivotal role in orchestrating ongoing inflammatory immune responses has been bolstered by several fairly newly described effector mechanisms, particularly their capacity to serve as a source of cytokines. This frequently neglected phenomenon is acquiring more and more credit and, as a result, our understanding of the molecular basis of neutrophil-derived cytokines has grown tremendously in the past 20 years. It is now clear that cytokine secretion by neutrophils is controlled by sophisticated regulatory mechanisms. In this issue of the European Journal of Immunology, Mankan et al. (Eur. J. Immunol. 42: 710-715) further extend our knowledge by reappraising the role of the inflammasome pathway, specifically the NLRP3 sensor, in the secretion of mature IL-1β by murine neutrophils. Accordingly, Mankan et al. (Eur. J. Immunol. 42: 710-715) identify the neutrophil expression of the NLRP3 inflammasome complex, and by using specific knockout mice, they also show that, in LPS-primed neutrophils, the NLRP3/ASC/caspase-1 axis plays a nonredundant role for IL-1β processing in response to typical NLRP3 inflammasome stimuli.