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Methyltransferase-like 3 (Mettl3) is a component of methyltransferase complex that mediates m6A modification of RNAs, and participates in multiple biological processes. However, the role of Mettl3 in cardiac electrophysiology remains unknown. This study aims to explore the ventricular arrhythmia susceptibility of Mettl3+/– mice and the underlying mechanisms. Mice were anesthetized with 2% avertin (0.1 mL/10 g body weight) for echocardiography and programmed electrical pacing. Whole-cell patch clamp technique was used to examine the electrophysiological property of cardiomyocytes. The expression of Cav1.2 was determined by qRT-PCR and western blot analysis. The m6A medication of mRNA was examined by MeRIP-Seq and MeRIP-qPCR. No differences are found in the morphology and function of the hearts between Mettl3+/– mice and wild-type (WT) controls. The QT and QTc intervals of Mettl3+/– mice are significantly longer. High-frequency electrical stimulation showed that heterozygous knockout of Mettl3 increases ventricular arrhythmia susceptibility. The whole-cell patch-clamp recordings showed that the APD is prolonged in Mettl3+/– ventricular myocytes and more EADs were observed. The density of ICa-L is substantially increased in ventricular myocytes of Mettl3+/– mice. The pore-forming subunit of L-type calcium channel Cav1.2 is upregulated in Mettl3+/– mice, while the mRNA of its coding gene CACNA1C does not change. MeRIP-Seq and MeRIP-qPCR showed that the m6A methylation of CACNA1C mRNA is decreased in cultured Mettl3-knockdown cardiomyocytes and Mettl3+/– hearts. Collectively, deficiency of Mettl3 increases ventricular arrhythmia susceptibility due to the upregulation of Cav1.2 by reducing m6A modification on CACNA1C mRNA in mice. This study highlights the role of m6A modification in the regulation of cardiac electrophysiology.