Ho et al. (2007) have reported that emodin blocked the binding of S protein to ACE2 and reduced the infectivity of S protein pseudo-typed retrovirus to Vero E6 cells. Emodin effectively blocked the interaction between S protein and ACE2 in a dose-dependent manner with IC50 of 200 μM, indicating it might be a potential therapeutic agent for the treatment of SARS. This evidence concerns the gene PROS1 and severe acute respiratory syndrome.