It was also suggested that when the human synovial membrane is exposed to hypoxic conditions or excessive glycolysis in multiple cells, copper death may be inhibited, leading to excessive survival and proliferation of various immune cells such as fibroblast-like synoviocytes, effector T cells and macrophages, further leading to inflammatory responses and bone destruction in RA patients; Meanwhile, important regulatory genes of copper apoptosis such as PDHA1, DLAT, FDX1MTF1 and LIAS have been shown to be closely associated with the RA process (23). The gene discussed is LIAS; the disease is rheumatoid arthritis.