Studies showed aging can disrupt this balance, leading to osteoporosis characterized by significantly increased FAP activity and decreased OLN levels.[8, 19] Additionally, a senescent pathogenic cell cluster in osteoarthritis features FAP dysfunction, whereas FAP overexpression promotes chondrocyte senescence and the senescence‐associated secretory phenotype (SASP).[20] Hence, cellular senescence might play a role in regulating FAP function.[21] However, the underlying mechanism by which cellular senescence influences the balance between FAP and OLN needs further elucidation. This evidence concerns the gene FAP and osteoporosis.