While Ras and Cdc42 were not altered as a result of subendothelial CC deposition, RhoA activity was enhanced and Rac1 activity was suppressed (both known to be associated with endothelial dysfunction) (Fig. 4h), indicating that the observed effects could at least partially be driven by alteration of RhoA/Rac1 activity. This evidence concerns the gene RAC1 and endothelial dysfunction.