In pathogenesis of diverse CVDs, such as hypertension and heart failure, CXCR3 promotes T cell polarization into effector Th1/Th17 cells, macrophage activation and Treg infiltration, which exacerbates pro-inflammatory response and cardiomyocytes injury.[33] Our findings uncover that exosome lncRNAs may drive CXCR3-mediated inflammatory response and lead to atrial structural remodeling and AF development. This evidence concerns the gene CXCR3 and atrial fibrillation.