**9. Conclusions**

Investigators and practitioners the world over are working toward a better understanding of the basis of degenerative joint diseases such as OA. Devising ways to alter or modify the relevant genes impacting the joint articular cartilage may lead to the development of successful, safe, and effective therapies to halt the progress, treat, or even prevent the occurrence of OA and other debilitating joint disorders in humans. CRISPR/Cas9, MSCs, EVs, and miRNAs may all play key roles in future treatments.

**Author Contributions:** Conceptualization, A.S.T. and J.T.O.; methodology, A.S.T. and J.T.O.; investigation, A.S.T.; writing—original draft preparation, A.S.T. and J.T.O.; writing—review and editing, C.K.F., A.G.C., J.T.O.; illustrations, S.M.F., M.J.H., A.G.C., and K.D.G.; supervision, J.T.O.; funding acquisition, J.T.O. All authors have read and agreed to the published version of the manuscript.

**Funding:** This research was funded by NIH NIGMS, grant number P20GM109095 and P20GM103408.

**Acknowledgments:** Authors wish to acknowledge support from the Institutional Development Awards (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health under Grants #P20GM103408, P20GM109095, and 1C06RR020533. We also acknowledge support from The Biomolecular Research Center at Boise State with funding from the National Science Foundation, Grants #0619793 and #0923535; the M. J. Murdock Charitable Trust; Lori and Duane Stueckle, and the Idaho State Board of Education.

**Conflicts of Interest:** The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.
