CFTR and cystic fibrosis: In a proof-of-conceptstudy, Henning et al. reported a covalent DUBTAC, EN523, that is capableof targeting noncatalytic allosteric C23 in the K48-ubiquitin-specificdeubiquitinase OTUB1 and recruiting OTUB1 to CFTR, a mutated and misfoldedprotein in cystic fibrosis. As a result,treatment of EN523 led to stabilized ΔF508-CFTR protein levelsand improved chloride channel conductance in human cystic fibrosisbronchial epithelial cells.