LPL and coronary artery disorder: To our knowledge, our study is the first to relate in a general population CHD incidence to genetic variation in MEOX2 and TCF15, two transcription factors that are highly expressed by cardiac endothelium and that in a heterodimeric fashion interfere with cardiac energy metabolism by driving endothelial CD36 and LPL expression, thereby facilitating fatty acid transport across the cardiac endothelium [3].