Cholesterol (>80 % in the form of cholesteryl esters (CE)) is transported by HDL from atherosclerotic plaque-associated macrophage foam cells to the liver by the process of reverse cholesterol transport (RCT), subsequently converted to bile acids (BA), and eliminated from bile/feces. Galactose-functionalized PAMAM dendrimer G5, i.e., Gal-G5, is developed as a hepatocyte-specific gene delivery system to deliver CEH expression vector. Galactose facilitates ASGPR-mediated endocytosis of Gal-G5/CEH complexes into hepatocytes in the liver and increases CEH expression. The overexpressed CEH would enhance the hydrolysis of HDL-CE into free cholesterol (FC), which is either directly secreted into bile or converted to bile acids followed by elimination from the body - a process proposed to regress the existing atherosclerotic plaques.