CLN3 and atrial fibrillation: Although the disruption of Cln3 expression was present in both AF+ and AF− cells in Cln3Δex7-8 mice, the latter subset was unaffected by the perturbation of the lysosomal pathway, suggesting that CLN3-dependent lysosomal degradation is dispensable in AF− microglia, which further highlights the molecular differences between AF+ and AF− microglia.