F508del-CFTR protein is prematurely degraded and when at the plasma membrane it displays a half-life much shorter than the wild type CFTR. F508del-CFTR can be partly rescued by corrector molecules, but a therapy to increment its stability seems to be a challenging issue for the therapeutic treatment of CF. Recent studies have shown that the protein CK2 is involved in the regulation of F508del-CFTR. According to experimental evidence of their previous project FFC#10/2016, researchers hypothesize that CK2 may affect F508del-CFTR stability at the level of Hsp27/Ubc9/SUMO/RNF4 QC pathway. So they will perform in cells assays (16-HBE and CFBE and primary human bronchial F508del-CFTR cells) to demonstrate that CK2 inhibition can decrease F508del-CFTR degradation. Since the so called proteostasis regulator cysteamine contributes by a different pathway to the F508del-CFTR rescue, the main aim of the project is to understand if the combination of inhibitors of CK2 with cysteamine or other CFTR correctors may achieve synergic or at least additive therapeutic effects.