Inhibition of DNM1L activity or expression reduces mitochondrial division, suppresses reactive oxygen species (ROS) expression, and alleviates murine autoimmune arthritis.[18] Here, we demonstrate that LACK156‐173 reduces the aggressiveness of RA‐FLSs and inhibits the de novo fatty acid synthesis pathway mediated by FASN. This evidence concerns the gene DNM1L and rheumatoid arthritis.