Finally, subchondral bone changes occur, where the activation of Stat3 in subchondral bone H-vessels leads to greater cell proliferation, migration, and angiogenesis, which may exacerbate the progression of OA (21).To provide a detailed view of the molecular mechanisms of CXCL8 and CXCL11 in osteoarthritis, Figure 2 depicts how these chemokines influence chondrocyte apoptosis and proliferation through the JAK/STAT3 signaling pathway. This evidence concerns the gene CXCL11 and osteoarthritis.