Persistent lung inflammation is a major cause of decline in respiratory function in cystic fibrosis (CF) patients. In this context, activation of integrin-mediated adhesion modulates polymorphonucleates (PMNs) pro-inflammatory recruitment into the lung. Researchers discovered that integrin activation in monocytes is regulated by CFTR protein, so that it is severely impaired in CF, where an unbalanced and excessive recruitment of PMNs into the lung parenchyma, is observed. Relying on these data they hypothesize that restoration of CFTR function by new modulators drugs restores also the activation of the main integrine called LFA-1 (Lymphocyte function-associated antigen) in CF monocytes. Thus, quantification of LFA-1 activation in monocytes may represent a specific marker of CFTR activity and can be exploited to monitor the efficacy of CFTR-correcting compounds. Peripheral blood samples from a minimum of 10 controls and 10 selected CF patients for each type II or III mutations, before and after therapy, will be obtained. Quantification of integrin activation will be evaluated by flow cytometry and in standard adhesion assays. The new approach, exploiting minimally invasive blood samples and highly sensitive assays, has the potential of becoming a new tool to improve predicting and monitoring clinical efficacy of novel CFTR corrector/potentiator therapies, thus allowing a personalized approach to CF treatment.