In OA, persistent activation of the pathway exacerbates cartilage inflammation and matrix degradation; In RA, persistent activation of the cGAS–STING pathway links aberrant self-DNA sensing with chronic synovial inflammation and joint destruction, highlighting its critical role in autoimmune bone erosion; in OP, dysregulated signaling contributes to the imbalance between bone formation and resorption; and in IVDD, the cGAS–STING pathway promotes cellular senescence, apoptosis, and inflammation, accelerating extracellular matrix degradation and annulus fibrosus damage. Here, STING1 is linked to rheumatoid arthritis.