SLC16A3 and rheumatoid arthritis: In RA synovium—where intra-articular acidosis is more pronounced—fibroblast-like synoviocytes up-regulate MCT4 (SLC16A3), and genetic or siRNA inhibition of MCT4 reduces inflammatory readouts and disease activity in vivo, establishing a mechanistic precedent for lactate-driven acidification of the joint space [34].