Background/Rationale. Deletion of phenylalanine 508 in CFTR (F508del) is the most common mutation in Cystic fibrosis (CF) patients (70-90%). F508del-CFTR maintains channel activity, but the mutation causes the majority of CFTR protein to be retained in the endoplasmic reticulum and prematurely degraded by the ubiquitin-proteasome system before it reaches the plasma membrane. The combination of lumacaftor-ivacaftor (corrector plus potentiator, OrkambiTM) represents the first FDA-approved therapy for CF patients homozygous for F508del-CFTR mutation, and in general a combination of therapy seems to show improved clinical benefits over available monotherapies (1). CK2 has been suggested as a potential target to rescue the membrane restoring autophagy while epigallocatechin gallate, selected for its ability to target the protein kinase CK2, sustains its permanence at the plasma membrane, even if not able alone to rescue F508del-CFTR (2).