With cardiac specific deletion of Centromere Protein F (CENP-F), a protein known to interact with microtubules6–8, the resulting animals exhibited enlarged ventricles with thinner walls, fewer trabeculae, increased fibrosis, and arrhythmia (all hallmarks of DCM), as well as death in 20% of outcomes5. Here, CENPF is linked to Arrhythmia.