EAT may play a pathogenetic role in heart dysfunction by secreting pro-fibrotic factors such as Activin A (known to be involved in heart failure pathogenesis) [14, 45] and cardio-depressant mediators such as FABP4 [46], by promoting cardiomyocyte apoptosis through local increase of intra-myocardial fatty acids, oxidative stress and inflammation [47]. Here, FABP4 is linked to heart failure.