Blocking CXCL12/CXCR4 axis with ADMD3100, a specific antagonist of CXCR4, can significantly suppress atrial structural remodeling and AF susceptibility, through inhibiting pro-fibrosis signaling (ERK1/2 and AKT/mTOR) and inflammatory response (infiltration of CD3+ T lymphocytes and F4/80+ macrophages). The gene discussed is MTOR; the disease is atrial fibrillation.