To further investigate the molecular mechanism by which Listerin regulates atherosclerosis progression and clarify the role of ABCA1 in this process, we conducted adenovirus-mediated overexpression of ABCA1 or its Listerin-targeted ubiquitination site mutant (K1884R/K1957R) in macrophage-specific Listerin-KO mice to determine whether ABCA1 reconstitution could counteract the proatherogenic effects of Listerin deficiency. This evidence concerns the gene LTN1 and atherosclerosis.