Therefore, using the pyrazone PYR-41 (23, Figure 13), a previouslyreported E1 inhibitor used in cancer therapy,132 Brodsky and co-workers showed that it is possible to significantlyincrease F508del-CFTR stability, trafficking to, and activity at thePM when a E1 inhibitor is combined with different types of correctors.133 However, the use of 23 is limiteddue to its toxicity, perhaps linked to its 5-nitrofuroyl moiety. This evidence concerns the gene CFTR and cancer.