In addition, Jing revealed that immunoglobulin G (IgG) stimulation of human and murine macrophages results in the production of numerous proinflammatory mediators, including IL-1β, which is dependent on HIF-1α and mTOR signaling, leading to metabolic reprogramming and subsequently driving inflammation in AIDs, such as RA, SLE, SSs, Sjögren’s syndrome (SS) and vasculitis (76). This evidence concerns the gene HIF1A and systemic lupus erythematosus.