**5. Conclusions**

During the last years, numerous important advances have led to a better understanding of EO's metabolisms and functions, including the characteristics of its receptor and the molecular effects of its activation. Although many important areas need to be further investigated, compelling data reinforce the concept that high EO plasmatic levels and adducin polymorphism (Gly460Trp) are associated with an increased risk of developing diseases including hypertension, ADPKD and organ complications, such as podocyte injury, cardiac and kidney hypertrophy. It also contributes to the development and the maintenance of AKI in critically ill patients.

The importance of these evidences is that the understanding of the patho-physiological mechanism undergoing complex diseases represents a valid substrate to individuate specific pharmacological targets. This is mainly important in complex multifactorial disease, when a tailored approach based on individuals' phenotypes and genotypes should be chosen to treat individual patients carrying a specific genetic background. Rostafuroxin might be considered to be a revolutionary therapy for hypertension when increased EO circulating levels and adducin polymorphism exert a pathogenetic role. Rostafuroxin perfectly fits the new concept of personalized medicine, and it can be considered to be a safe drug without the most common side effects of previous used compounds.

**Author Contributions:** Conceptualization: P.M., M.S., L.C., C.L.; methodology: E.M., P.C.; software: L.C.; validation: E.M.; formal analysis: C.L.; investigation: M.S.; resources and data curation: all the authors; writing of the original draft preparation: P.M., M.S., P.C.; writing of review and editing: P.M., P.C.; visualization: all the authors; supervision: P.M.; project administration: P.M.

**Funding:** This research received no external funding.

**Conflicts of Interest:** The authors declare no conflicts of interest.
