Beyond the inherent advantages of EVs, such as their nanoscale size facilitating barrier penetration, lower immunogenicity enabling allogeneic use, and reduced risk profile compared to live cells (e.g., avoiding uncontrolled differentiation or malignant transformation) [17, 19], our findings highlight the ​​CCR2‐dependent targeting capability​​ as a defining feature of GMSC‐EVs for RA. Here, CCR2 is linked to rheumatoid arthritis.