demonstrated that increasing the content of Ang‐(1–7) through ACE2 activation ameliorated functional, radiological, and histopathological alterations in a knee osteoarthritis rodent model.[38] Nevertheless, to the best of our knowledge, the pathological role of the ACE2/Ang‐(1–7) axis in NPC senescence and IVDD progression has yet to be elucidated. This evidence concerns the gene ACE2 and osteoarthritis, knee.