This differs from the previous toxic effects of ASIC1a in synovial inflammation, and there are many reasons for this contradiction, the most important of which may be the differences between ASIC isoforms that lead to this effect, the different cell types used, etc. To better understand the therapeutic opportunities that the ASIC3 channel provide in RA, a number of studies will be needed in the future to validate the impact of different modalities of modulation on RA. The gene discussed is ASIC1; the disease is rheumatoid arthritis.