Moreover, aged wild-type mice, infected with AAV9-Tert, present improved mitochondrial fitness, with partial rescue of PGC-1α, ATP synthase, and ERRα expression in the heart [192], and they are protected from heart failure after myocardial infarction (MI), with restored metabolic activity in the infarcted hearts [192,193] (Table 1). The gene discussed is TERT; the disease is myocardial infarction.