In line with these studies, our study observed that miR-126-5p high expression was an independent predictive factor for longer MACCE-free survival, which might due to: miR-126-5p promoted endothelial proliferation through repressing Notch1 inhibitor delta-like 1 homolog (Dlk1) and facilitated VEGF signaling via suppressing SPRED1 and PIK3R2/p85-β, thereby decreased endothelial dysfunction and repressed coagulation to prevent formation of atherosclerotic lesion, thus reduced MACCE risk and led to better MACCE-free survival in CAPD patients [23, 26]. The gene discussed is DLK1; the disease is endothelial dysfunction.