Abdominal aortic aneurysms (AAA) usually progress asymptomatically and are undetected until rupture occurs. Once ruptured, the mortality rate of AAA is about 80 %. Among all patients with ruptured AAA, about one-third die without reaching hospital, and about another quarter reach hospital but die prior to surgical intervention. Among the remaining patients (about 40 %) surviving AAA rupture long enough to benefit from surgical intervention, the perioperative mortality has historically reached about 50 % [1], a value that has however recently decreased owing to the introduction of endovascular repair [2]. On the other hand, elective AAA repair has a much lower in-hospital mortality rate, with recently reported values of 1.3 % and 4.7 % for endovascular and open surgical repair, respectively [3], thereby strongly emphasizing the need for screening and identification of those patients with prone-to-rupture AAA.The crude estimate of AAA diameter remains the most widely used predictive risk factor for AAA rupture and the sole therapeutic management criterion. Indeed, in both the 2014 European Society of Cardiology and the 2011 American College of Cardiology/American Heart Association guidelines, aortic repair is a class I indication if the AAA diameter exceeds 55 mm [4,5]. However, the limitations of this parameter are well acknowledged, and it is therefore unanimously agreed that a more robust noninvasive predictor of the individual risk of AAA rupture is required. Although being much less documented than atherogenesis, the current knowledge regarding the pathophysiology of AAA indicates that parietal inflammation, matrix degradation and smooth muscle cell apoptosis are required for AAA pathogenesis [6]. FDG has been suggested as a potentially useful agent for the molecular imaging of vascular inflammation due to the elevated carbohydrate metabolism of extravasated inflammatory cells [7]. As such, the tracer has been extensively evaluated in both the experimental and clinical settings for the noninvasive imaging of inflammatory processes in vulnerable atherosclerotic lesions as well as in AAA.In the multicentre study by Barwick and colleagues published in this issue of the European Journal of Nuclear Medicine & Molecular Imaging [8], the authors used PET imaging of FDG uptake to retrospectively compare the metabolic activity in the abdominal aortic wall of 151 patients with AAA (mean aortic diameter, 50±13 mm) with that of 159 individuals with no AAA (mean aortic diameter, 21±3 mm) and matched for age, sex, diabetes, smoking status, statin use and indication for PET/CT. This cohort is the largest so far used for the comparison of FDG uptake between AAA and normal vessels in well-matched patients. FDG uptake was analysed by semiquantitative visual scoring as well as quantitatively using SUVmax and target to background ratios utilizing mediastinal blood pool or descending thoracic aorta activities for normalization. Although the retrospective nature and the design of the study limit the conclusions that can be drawn w...