When Ace2 is transgenically overexpressed in mouse heart, cardiac defects are again observed, most notably a lethal ventricular arrhythmia, which is associated with disruption of gap junction formation [9Donoghue M et al.Heart block, ventricular tachycardia, and sudden death in ACE2 transgenic mice with downregulated connexins.J. Mol. Cell. Cardiol. 2003; 35: 1043-1053Abstract Full Text Full Text PDF PubMed Scopus (142) Google Scholar]. The high incidence of sudden death in these mice correlated with the levels of Ace2 transgene expression. Surviving older mice showed a spontaneous downregulation of the transgene and restoration of normal cardiac function.