Furthermore, 4′-diisothiocyano-2,2′-stilbenedisulphonate (DIDS)-mediated MCT1 inhibition not only blocks lactate efflux (199) but also impairs MCT1-dependent lactate uptake by CD4+ T cells, CD8+ T cells, and FLS in RA, thereby disrupting pro-inflammatory metabolic signaling and alleviating joint inflammation (Table 1). Here, CD8A is linked to rheumatoid arthritis.