A study found SEA-0400 to be antiarrhythmic in mouse models with increased NCX expression, such as HF and AF, but in conditions with reduced NCX expression, SEA-0400 was found to increase Ca2+ transient amplitude and spontaneous Ca2+ transients, ultimately acting proarrhythmic (Bogeholz et al., 2017). This evidence concerns the gene TLX2 and atrial fibrillation.