Interestingly, we found the following evidence to suggest that ARID5B might be involved in monocyte subset regulation: (i) HL and HHcy could trigger cg25953130 hypermethylation and decrease ARID5B expression in CAD patients and ox-LDL- and Hcy-treated primary monocytes; (ii) ARID5B was associated with increases in nonclassical and decreases in classical monocyte proportions; and (iii) ARID5B was negatively associated with the expression of CCR2, which was upregulated in intermediate monocytes. Here, CCR2 is linked to coronary artery disorder.