As expected, WT endothelial cells showed a clear punctate pattern of DiI-oxLDL, characteristic of a vesicular uptake mechanism, whereas deletion of Cav-1 resulted in a significant decrease in oxLDL uptake, which was fully rescued by infection of Cav-1 KO cells with an adenoviral vector expressing Cav-1 (Fig. 1D). Here, CAV1 is linked to infection.