CF patients have severe clinical complications that affect several organs, including intestine, pancreas and liver. The most affected target is however the respiratory system, in which the reduced activity of the CFTR channel results in obstruction of small airways that, together with airway inflammation and infections. Researchers hypothesize that the enzyme phosphoinositide 3-kinase (PI3Kγ) critically controls the function of the multitude of cell types that are central to CF development. Therefore, they intend to explore whether PI3Kγ inhibition represents a suitable approach to both correct the primary defect of the disease (CFTR hypofunction) and limit the disease-associated complications (airway inflammation and hyperresponsiveness). They will investigate whether PI3Kγ inhibition provides therapeutic benefits in cell-based and pre-clinical models of CF. In particular, they intend to examine whether a molecule targeting PI3Kγ activity corrects the primary cause of CF by potentiating the activity of the mutant channel in epithelia. In addition, they plan to explore whether the same compound is effective in inhibiting leukocyte activation, thus reducing the uncontrolled lung inflammation that typically occurs in CF patients. Finally, they intend to evaluate the ability of the molecule to serve as bronchodilator and thus alleviate CF-associated bronchial hyperresponsiveness. The use of PI3Kγ inhibitors may both correct the primary defect of the disease and limit the associated complications such as pulmonary inflammation.