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The sodium channel Na_V1.8, encoded by the <i>SCN10A</i> gene, has recently emerged as a potential regulator of cardiac electrophysiology. We have previously shown that Na_V1.8 contributes to arrhythmogenesis by inducing a persistent Na⁺ current (late Na⁺ current, I_NaL) in human atrial and ventricular cardiomyocytes (CM). We now aim to further investigate the contribution of Na_V1.8 to human ventricular arrhythmogenesis at the CM-specific level using pharmacological inhibition as well as a genetic knockout (KO) of <i>SCN10A</i> in induced pluripotent stem cell CM (iPSC-CM). In functional voltage-clamp experiments, we demonstrate that I_NaL was significantly reduced in ventricular <i>SCN10A</i>-KO iPSC-CM and in control CM after a specific pharmacological inhibition of Na_V1.8. In contrast, we did not find any effects on ventricular APD₉₀. The frequency of spontaneous sarcoplasmic reticulum Ca²⁺ sparks and waves were reduced in <i>SCN10A-</i>KO iPSC-CM and control cells following the pharmacological inhibition of Na_V1.8. We further analyzed potential triggers of arrhythmias and found reduced delayed afterdepolarizations (DAD) in <i>SCN10A-</i>KO iPSC-CM and after the specific inhibition of Na_V1.8 in control cells. In conclusion, we show that Na_V1.8-induced I_NaL primarily impacts arrhythmogenesis at a subcellular level, with minimal effects on systolic cellular Ca²⁺ release. The inhibition or knockout of Na_V1.8 diminishes proarrhythmic triggers in ventricular CM. In conjunction with our previously published results, this work confirms Na_V1.8 as a proarrhythmic target that may be useful in an anti-arrhythmic therapeutic strategy.