The present study also has limitations, including: i) a focus on the mechanism of ATF6α-mediated activation and maintenance of RA-FLSs, which does not exclude the possibility that ATF6α may also promote arthritic progression by influencing other immune cell functions (e.g., T cells, macrophages, and regulatory T cells; ii) no profiling of targeted genes through ChIP-sequencing, which warrants further studies; iii) the sample size of the RA patient study was small, so the results may not be fully generalizable. This evidence concerns the gene ATF6 and rheumatoid arthritis.