BCP mitigated hypercholesterolemia, dyslipidemia, and vascular inflammation, reduced atherogenic and coronary risk index, and corrected lipid metabolism by inhibiting proatherogenic vascular cell adhesion molecule 1 (VCAM-1) and restoring vascular eNOS/iNOS expression by maintaining the NO levels, mediating the activation of CB2 and PPAR-γ receptors in a high-fat diet and fructose-induced obesity (Baldissera et al., 2017; Harb et al., 2018; Youssef et al., 2019). The gene discussed is VCAM1; the disease is Hypercholesterolemia.