Based on the initial assumption that SK4 K+ channels are proarrhythmic and proinflammatory, in this study, we examined whether atrial SK4 channels are upregulated in the post-MI setting in rats and whether their blockade using our recently developed allosteric inhibitor BA6b9 could mitigate the AF substrate and atrial remodeling that develop in this HFrEF model, which mimics important aspects of MI and AF comorbidity in humans (36, 50, 51). This evidence concerns the gene KCNN4 and atrial fibrillation.