Interestingly, when cardiomyocytes-specific PPARγ-overexpressing mice were crossed with PPARα-deficient mice, cardiac hypertrophy was significantly ameliorated, along with upregulated FAO and decreased apoptosis, reactive oxygen species (ROS) levels, and endoplasmic reticulum stress (Son et al., 2010). The gene discussed is PPARA; the disease is cardiac hypertrophy.