showed the NLRP3 mitochondrial recruitment and activation in CF airway cells during P. aeruginosa infection, since defective CFTR induced mitochondrial Ca2+-overload and ROS production, which in turn driven the NLRP3 inflammasome activation and release of IL-1β and IL-18 (Rimessi et al., 2015). This evidence concerns the gene IL1B and cystic fibrosis.