The reason for the specific responsiveness of HCAEC to different drugs, contrary to other types of cells, could be that the endothelium of arteries (versus veins) exhibits (a) specific and intrinsic expression patterns and unique response profiles leading to inflammation and atherosclerosis and (b) greater susceptibility of HCAEC to inflammatory stimuli, specifically pathological concentrations of SAA and IL-1β, as opposed to HUVEC and HMVEC [17, 18]. This evidence concerns the gene SAA1 and atherosclerosis.