Likewise, low density lipoprotein receptor (ldlr) knock out mice (model for atherosclerosis) with a deletion of either IL23 or IL-22 in the bone-marrow derived cells (immune cells) exhibited reduced intestinal barrier function and increased epithelial adherent bacteria including Clostridiaceae and Ruminococcaceae, causing systemic increase in lipopolysaccharide (LPS) and trimethylamine N-oxide (TMAO) associated with development of atherosclerosis (Fatkhullina et al., 2018). This evidence concerns the gene IL23A and atherosclerosis.