It has been shown that, in vitro, the exposure of human macrophages to lipopolysaccharide induces histone H3 acetylation on lysines 9 and 27 (H3K27ac, H3K9ac), enhancing HAT1 expression, which in turn, promotes Nox5 gene promoter activity leading to reactive oxygen species overproduction in atherosclerosis [41]. Here, NOX5 is linked to atherosclerosis.