In addition, the peroxisome proliferator-activated receptor γ (PPARγ) and HIF1α in human and mouse cardiac hypertrophy activated FAs uptake and GPL biosynthesis genes, and increased glucose-to-GPL conversion via G-3P pathway followed by changing myocardial metabolism and forming heart disease (Krishnan et al., 2009). This evidence concerns the gene HIF1A and cardiac hypertrophy.