A crucial downstream effector molecule of HIF-1α, vascular endothelial growth factor-α (VEGF-α), can trigger endothelial cell activation, proliferation, and migration, leading to neovascularization.[9] Thus, inhibiting the activation of the HIF-1α/VEGF-α signaling pathway could potentially improve the pathogenic neovascularization associated with OA.[10] One of the pathological characteristics of OA is synovitis, and the joint cavity’s hypoxic microenvironment is the condition it is in. This evidence concerns the gene HIF1A and synovitis.