Trikafta, despite undoubtedly representinga breakthrough in CF treatment by significantly slowing down CF progresswith substantiated clinical benefits,31 fails to fully restore mutant CFTR function.26,32 As an example, treatment with Trikafta reduces only partially theubiquitylation status of F508del-CFTR.32 Therefore, both academies and pharmaceutical companies have beeninvolved in searching for small-molecule correctors33 and potentiators34 with differentmechanisms or with ameliorated characteristics. This evidence concerns the gene CFTR and cystic fibrosis.