On the other hand, it was found that RA was closely related to splicing variants (59, 60), and by examining the altered levels of splicing mechanism components and inflammatory mediators, it was found that the dysregulation of splicing mechanism components, such as SNRNP70, SNRNP200 and U2AF2, could be reversed when TNFi was intervened in vivo (61). This evidence concerns the gene SNRNP70 and rheumatoid arthritis.