We previously showed that oxidation of HDL ex vivo with peroxidase-generated tyrosyl radical (tyrosylated HDL or tyrHDL) increases the ability of HDL to deplete the regulatory pool of intracellular cholesterol [6], increase cholesterol available for subsequent efflux to apoA-I and other lipid acceptors [7], and reduce the development of atherosclerosis in apoE-deficient mice [8]. This evidence concerns the gene APOA1 and atherosclerosis.