In FLS from RA, the unregulated MALAT1 is associated with increased cell apoptosis, and the knockdown of MALAT1 inhibits the apoptosis of FLS by suppressing the expression of caspase-3 and caspase-9 (84), suggesting that MALAT1 contribute to the pathogenesis of RA through regulating apoptosis. This evidence concerns the gene CASP3 and rheumatoid arthritis.