Furthermore, when combined with the corrector 2, 11 was able to efficiently correct the traffickingdefect of F508del-CFTR and boost the mutant channel activity.81 However, compound 11 was withdrawnfrom phase 1 clinical study due to its poor metabolic stability.82 Since then, many researchers have been lookingfor analogues of 11 with a similar effect on Hsc70 andimproved safety and pharmacokinetic profiles.83,84 Despite that, an analysis of the efficacy of those new Hsc70 inhibitorson CFTR rescue is still missing, and we believe that it could be ofgreat interest for the CF community. Here, HSPA8 is linked to cystic fibrosis.