A-FABP4 is also implicated in the development of insulin resistance and atherosclerosis in animal studies. In A-FABP knockout mice with comorbid leptin deficiency, the animals became obese compared with those with control mice with leptin deficiency only. Insulin sensitivity, however, improved significantly in the A-FABP knockout mice despite their obesity. In an A-FABP and ApoE double-knockout mouse model, the mean atherosclerotic lesion area in the aorta decreased by 66% in double-knockout mice compared with controls. Recently, several clinical studies have demonstrated an association between A-FABP and coronary atherosclerosis. In a report by Jin et al., the A-FABP concentration was higher in female CAD patients than in nonCAD subjects and was also independently associated with Gensini scores. Circulating A-FABP concentrations were significantly higher in patients with CAD. In a multivariate logistic regression analysis, A-FABP concentration was an independent predictor for CAD in women even after adjusting for waist circumference, HbA1c, insulin resistance, LDL, glomerular filtration rate, and N-terminal pro-brain natriuretic peptide. Our results complement these studies and show that A-FABP is not only associated with the presence of CAD but also significantly associated with the presence of clinically significant ischemia. The association remained significant after adjusting for age, blood pressure, and history of CAD. This association was significant in the total participant group and in women but not in men. Although the small patient number in the present study may be responsible for the differences in associations between women and men, a gender-dependent association was also observed in the results of Bao et al.. It is well known that body fat distribution, abdominal adipose tissue in particular, differs between human males and females. Women have less visceral fat accumulation and a lower ratio of VAT to total body fat compared with men. Sexual dimorphism has also been reported for adipokines, including leptin, adiponectin, and chemerin. These gender differences in adipokines may reflect gender differences in adipocyte function or sex hormone regulation. Our results corroborate previous reports, suggesting that A-FABP may have a more prominent role in the pathogenesis of myocardial ischemia in females compared with males. In addition, A-FABP may be involved in atherosclerosis during the advanced stages, when a considerable amount of myocardium is at risk. We tested the potential clinical use of A-FABP or chemerin in identifying patients with significant ischemia. Current guidelines utilize the presence of significant ischemia as one of the factors that determine if a patient with CAD needs to receive percutaneous coronary intervention. Patients with larger areas of ischemic myocardium are at higher risk for future cardiovascular events, and thus benefit from revascularization.