Administration of lumacaftor/ivacaftor to pwCF homozygous for F508del mutations was also shown to increase the key metabolic checkpoint molecule PTEN levels in PBMCs [183], suggesting that highly effective CFTR modulator therapy will shift cellular metabolism in vivo to a less inflammatory state [170], therefore tuning down the characteristic hyperinflammatory disease state associated with CF-ABPA. Here, CFTR is linked to cystic fibrosis.