EVs isolated from serum samples of AF patients carried MIAT to bind to miR‐485‐5p and caused the upregulation of the miR‐485‐5p target CXCL10, inducing atrial myocyte fibrosis, inflammation, and oxidative stress, thus promoting atrial remodeling and aggravating the AF. Here, CXCL10 is linked to atrial fibrillation.