In functional studies, PARP inhibition or deletion could lead to an increase in collagen content (Oumouna-Benachour et al., 2007), the prevention of dyslipidemia-induced endothelial dysfunction (Hans et al., 2009a), and the reduction in plaque sizes and numbers (Oumouna-Benachour et al., 2007; von Lukowicz et al., 2008; Hans et al., 2009a), suggesting the key roles of PARP activities in plaque progression (Oumouna-Benachour et al., 2007). The gene discussed is PARP1; the disease is metabolic syndrome.