Previous studies have also examined the effects of CFTR corrector therapy on inflammasome activation and found that monocytes from individuals treated with ETI demonstrated decreased expression of the P2 × 7 receptor, which promotes ATP-induced inflammasome activation, and were more resistant to inflammasome activation than monocytes from the same individuals before receiving ETI [181]; tezacaftor/ivacaftor treatment has been linked to similar changes in inflammasome activation in a study of PBMCs from patients with CF homozygous for F508del mutations [182]. This evidence concerns the gene CFTR and cystic fibrosis.