Unlike in the ALK1-deficient model highlighted above, another postmortem study found that mural cell coverage was infrequent in microvessels in both normal and atherosclerotic vessels. 19 This suggests that in atherosclerosis, mural cell coverage is likely not the defect causing increased vascular permeability. Rather this particular study found that plaque microvessels had abnormal morphology, aberrant endothelial cell junctions, and leukocyte adherence. Bobryshev et al20 found abnormal endothelial cell VE-cadherin expression associated with areas of inflammation in human carotid plaques, suggesting the link between inflammation and endothelial incompetence. Thus, the mechanisms of vessel incompetence in atherosclerosis remain incompletely understood but may involve interactions between immune cells and the endothelium.