The ability of HDL to support cholesterol efflux is also modulated in individuals with the metabolic syndrome, particularly via SR‐BI and ABCG1 pathways, indicative that a multitude of steps in reverse cholesterol transport are reduced in the setting of cardiometabolic disease.26 Our study has shown that the microenvironment of obese adipose tissue results in increased ABCA1 activity, in contrast to peripheral cells from diabetic patients, again indicative that the primary source of tissue macrophages is a critical determinant of cellular ABCA1. Here, ABCA1 is linked to metabolic syndrome.