In our study, it was demonstrated that stable atherosclerotic plaques at the stage of lipidosis and fibrosis were characterized by increased amounts of cytoskeletal proteins such as actin, tropomyosin, tubulin, MAGP-4, and vimentin; this alteration is apparently associated with cellular migration to the subendothelial space after damage to the vessel wall (during subsequent inflammation). This evidence concerns the gene DNM2 and lysosomal lipid storage disorder.