We hypothesize that the subclinical cardiomyocyte injury caused by AF can activate the CXCL12/CXCR4 axis to promote atrial tissue repair, while the hyperactivation of CXCL12/CXCR4 axis seems to be more conducive to the formation of AF substrates, thereby contributing to AF maintenance [53, 54]. This evidence concerns the gene CXCR4 and atrial fibrillation.