Studies demonstrated that the incidence of atrial fibrillation is significantly increased in patients with diabetes mellitus. Increase of late sodium current (I_NaL) has been associated with atrial arrhythmias. However, the role of I_NaL in the setting of atrial fibrillation in diabetes mellitus remained unknown. In this study, we investigated the alteration of I_NaL in the atria of diabetic mice and the therapeutic effect of its inhibitor (GS967) on the susceptibility of atrial fibrillation. The whole-cell patch-clamp technique was used to detect single cell electrical activities. The results showed that the density of I_NaL in diabetic cardiomyocytes was larger than that of the control cells at the holding potential of −100 mV. The action potential duration at both 50% and 90% repolarization, APD₅₀ and APD₉₀, respectively, was markedly increased in diabetic mice than in controls. GS967 application inhibited I_NaL and shortened APD of diabetic mice. High-frequency electrical stimuli were used to induce atrial arrhythmias. We found that the occurrence rate of atrial fibrillation was significantly increased in diabetic mice, which was alleviated by the administration of GS967. In GS967-treated diabetic mice, the I_NaL current density was reduced and APD was shortened. In conclusion, the susceptibility to atrial fibrillation was increased in diabetic mice, which is associated with the increased late sodium current and the consequent prolongation of action potential. Inhibition of I_NaL by GS967 is beneficial against the occurrence of atrial fibrillation in diabetic mice.