The results showed that several compounds increased F508del-CFTRmaturation, expression, and activity at nanomolar concentrations.In particular, inhibitors of the receptor Tyr kinases (FGFRs, VEGFR,and PDGFR), such as the indolinone SU5402 (54, Figure 24) and its analogueSU6668 (55, Figure 24), already in clinical trials mainly for cancer therapy,showed a robust rescue of the mutant CFTR channel.214 However, how the identified kinase inhibitors could possiblyrescue F508del-CFTR needed further investigations. The gene discussed is CFTR; the disease is cancer.