Different components of inflammasome were studied and it was shown that NLRP3 more than NLRC4 contributed to pathogenic inflammatory responses in murine and human CF epithelial cells; moreover, it correlated with lower levels of IL-1Ra production and reduced NLRC4 activation. Pathogenic NLRP3 activity could be negatively regulated by IL-1Ra and this provide a proof-of- concept evidence that IL-1Ra may limit the pathological consequences of microbial colonization in CF. Genetic analysis supported the role of NLRC4 and IL-1Ra in determining the state of microbial colonization in CF patients. These promising results highlight the possibility of repurposing Anakinra as a therapeutic strategy in FC.