Given that cardiomyocytes are the most mitochondria-rich cells in the body and depend heavily on oxidative metabolism for sustained contractility, we reasoned that activation of mitochondrial biogenesis and lipid metabolism via the AMPK/PGC-1α axis may be a compensatory response to infection that could be harnessed for therapeutic benefits if activated earlier in the course of disease. The gene discussed is PPARGC1A; the disease is infection.