The interaction of rhPRG4 and CD44 on the surface of rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS) results in inhibition of nuclear factor kappa B (NFκB) nuclear translocation and inhibition of proinflammatory-cytokine-induced RA-FLS proliferation [18]. Here, CD44 is linked to rheumatoid arthritis.