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). The gene discussed is MTOR; the disease is systemic lupus erythematosus.