This included Uchl1, which encodes for a ubiquitin hydrolase that is upregulated in myocytes following myocardial infarction [36]; Slc25a20, which has been independently associated with rhythm status among patients with AF [37]; and Upc2, which influences the susceptibility for Ca2+-mediated arrhythmias, modulates myocardial excitation–contraction coupling, and attenuates oxidative stress [38,39,40]. Here, SLC25A20 is linked to myocardial infarction.