F508del-CFTR can be rescued to plasma membrane by corrector molecules, but a therapy to increments its stability is a key point. It was shown that the protein CK2 is involved in the regulation of F508del-CFTR stability, but the ultimate mechanism of action is not clear. Inhibition of CK2 has been suggested as a potential new tool in combination with the so called “proteostasis regulator” cysteamine to rescue the defective protein. The basis of a new therapy, based on CK2- inhibitors combined with cysteamine or correctors or potentiators will be studied, in order to point out CK2 protein role and additive/synergic effects of different combinations.