We elucidated several new mechanisms for pathogenesis of cardiovascular diseases. We had identified angiotensin converting enzyme 2 (ACE2), as an in vivo SARS-coronavirus receptor and demonstrated that ACE2 plays a crucial role in SARS pathogenesis (Nature 2005, Nat Med. 2005). We elucidated Apelin, a new peptide hormone as well as a substrate for ACE2 is a crucial regulator of heart contractility (Circ Res 2007) and recently demonstrated that Apelin - ACE2 - Angiotensin 1-7 axis is essential compensatory pathway in failing hearts (JCI 2013). In lipid library screening and metabolome analysis, we discovered Protectin D1, a lipid mediator, as a novel regulator of influenza virus RNA export, which suppresses influenza virus replication (Cell 2013). In genome-wide in vivo RNAi fly library screening (collaboration with IMBA), we identified CCR4-NOT complex, especially CNOT3 subunit, as a novel regulator of heart functions (Cell 2010). CCR4-NOT was originally isolated as a global transcription regulator from yeast mutants, and it has recently been shown as a crucial deadenylase for mRNA poly-A tail shortening. Currently, we hypothesize that CCR4-NOT complex is a global regulator of gene expression linking metabolism of mRNA and epigenetic gene regulation.