Figure 1e, shows that IL-1β release from quiescent lymphocytes was negligible, whether from HD or CLL subjects. Notably, LPS-stimulated release was about four fold lower in CLL lymphocytes than in HD PBMCs despite much higher P2X7R expression in the former cells. The P2X7R is tightly functionally associated to the NLRP3 inflammasome, the major intracellular apparatus responsible for IL-β processing and release2, therefore, we investigated whether ASC and NLRP3 expression paralleled P2X7R expression level, and thus was also increased in CLL lymphocytes. This evidence concerns the gene NLRP3 and B-cell chronic lymphocytic leukemia.