We confirmed a dysregulation of Na+ and K+ transport by examining primary innate immune cells and HBEC lines with CF-associated mutations in vitro and discovered that excessive ENaC-mediated Na+ flux, measured indirectly by dependent changes of fluorescence signal, correlate with an increased K+ efflux, an activating signal of the NLRP3 inflammasome and downstream IL-18 and IL-1β secretion. The gene discussed is NLRP3; the disease is cystic fibrosis.