Studies have demonstrated that activation of the JAK/STAT pathway contributes to the pathological progression of OA by regulating inflammation (Kaneko et al. 2000), immune responses (Yang et al. 2024a, b), mechanical load (Millward-Sadler et al. 2006), and apoptosis (Yang et al. 2016), ultimately leading to cartilage destruction, subchondral bone remodeling, and synovial inflammation (Zhou et al. 2022; Li et al. 2017). This evidence concerns the gene SOAT1 and inflammation.