To robustly test the efficiency and potential clinical translatability of PLN-ASO treatment in a variety of cardiac disease, covering the aforementioned aspects, we selected three different rodent HF models: two mouse DCM models, one driven by mutant PLN R14del, and the other driven by a Cspr3/Mlp−/− mutation, and a rat post-MI model to represent common acquired heart disease (Fig. 5. The gene discussed is PLN; the disease is myocardial infarction.