For CF, if initially CK2 inhibition had been suggested as a potential therapeutic intervention to potentiate the effect of proteostasis regulators for Phe508del-CFTR rescue,226 recent evidence suggests that CK2 activity is required for proper CFTR mutant maturation,224,229 and for the preservation of other ion channels that may compensate for CFTR dysfunctions.231. This evidence concerns the gene CFTR and cystic fibrosis.