The possible reasons were as follows: (1) CDC42 interacted with adenosine triphosphate binding cassette transporter A-I to promote cholesterol efflux in foam cells, which reduced the intracellular accumulation of cholesterol; thus, it was negatively correlated with TC and LDL-C in DCB-treated SV-CAD patients [24–26]. This evidence concerns the gene CDC42 and coronary artery disorder.