How can cholesterol efflux capacity be used as a risk factor for atherosclerotic cardiovascular disease?

While CEC is a promising surrogate marker, it remains a phenomenon rather than a therapeutic target, and there is no conclusive evidence that increasing CEC reduces ASCVD events. Future research should focus on disease-specific molecules, such as FABP5 and ORM1, that impair HDL function. Identifying these pathways may yield novel biomarkers and therapeutic targets, offering a more precise approach to residual cardiovascular risk beyond HDL-C levels.