Background: Patients with type 2 diabetes mellitus are at increased risk of cardiovascular disease, partly owing to dyslipidaemia, which can be amenable to fibrate therapy. We designed the Fenofibrate Intervention and Event Lowering in Diabetes(FIELD)study to assess the effect of fenofibrate on cardiovascular disease events in these patients. Methods: We did a multinational, randomised controlled trial with 9795 participants aged 50-75 years, with type 2 diabetes mellitus, and not taking statin therapy at study entry. After a placebo and a fenofibrate run-in phase, we randomly assigned patients(2131 with previous cardiovascular disease and 7664 without)with a total-cholesterol concentration of 3.0-6.5 mmol/L and a total-cholesterol/HDL-cholesterol ratio of 4.0 or more or plasma triglyceride of 1.0-5.0 mmol/L to micronised fenofibrate 200 mg daily(n=4895)or matching placebo(n=4900). Our primary outcome was coronary events(coronary heart disease death or non-fatal myocardial infarction); the outcome for prespecified subgroup analyses was total cardiovascular events(the composite of cardiovascular death, myocardial infarction, stroke, and coronary and carotid revascularisation). Analysis was by intention to treat. The study was prospectively registered(number ISRCTN 64783481). Findings: Vital status was confirmed on all but 22 patients. Averaged over the 5 years’study duration, similar proportions in each group discontinued study medication(10%placebo vs 11%fenofibrate)and more patients allocated placebo(17%)than fenofibrate(8%; p< 0.0001)commenced other lipid treatments, predominantly statins. 5.9%(n=288)of patients on placebo and 5.2%(n=256)of those on fenofibrate had a coronary event(relative reduction of 11%; hazard ratio[HR] 0.89, 95%CI 0.75-1.05; p=0.16). This finding corresponds to a significant 24%reduction in non-fatal myocardial infarction(0.76, 0.62-0.94; p=0.010)and a non-significant increase in coronary heart disease mortality(1.19, 0.90-1.57; p=0.22). Total cardiovascular disease events were significantly reduced from 13.9%to 12.5%(0.89, 0.80-0.99; p=0.035). This finding included a 21%reduction in coronary revascularisation(0.79, 0.68-0.93; p=0.003). Total mortality was 6.6%in the placebo group and 7.3%in the fenofibrate group(p=0.18). Fenofibrate was associated with less albuminuria progression(p=0.002), and less retinopathy needing laser treatment(5.2%vs 3.6%, p=0.0003). There was a slight increase in pancreatitis(0.5%vs 0.8%, p=0.031)and pulmonary embolism(0.7%vs 1.1%, p=0.022), but no other significant adverse effects. Interpretation: Fenofibrate did not significantly reduce the risk of the primary outcome of coronary events. It did reduce total cardiovascular events, mainly due to fewer non-fatal myocardial infarctions and revascularisations. The higher rate of starting statin therapy in patients allocated placebo might have masked a moderately larger treatment benefit. Background: Patients with type 2 diabetes mellitus are at increased risk of cardiovascular disease, partly due to dyslipidaemia, which can be amenable to fibrate therapy. We designed the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study to assess the effect of fenofibrate on cardiovascular disease events in these patients. Methods: We did a multinational, randomized controlled trial with 9795 participants aged 50-75 years, with type 2 diabetes mellitus, and not taking statin therapy at study entry. After a placebo and a fenofibrate run-in phase, we randomly assigned patients (2131 with previous cardiovascular disease and 7664 without) with a total-cholesterol concentration of 3.0-6.5 mmol / L and a total-cholesterol / HDL-cholesterol ratio of 4.0 or more or plasma triglyceride of 1.0-5.0 mmol / L to micronised fenofibrate 200 mg daily (n = 4895) or matching placebo (n = 4900). Our primary outcome was coronary events (coronary heart disease death or non-fatal myocardial infarction); the outcome for prespecified subgroup analyzes was was cardiovascular events (the composite of cardiovascular death, myocardial infarction, stroke, and coronary and carotid revascularisation). Analysis was by intention to treat. The study was prospectively registered (number ISRCTN 64783481). averaged over the 5 years’study duration, similar proportions in each group discontinued study (10% placebo vs 11% fenofibrate) and more patients allocated placebo (17%) than fenofibrate (8%; 5.9% (n = 288) of patients on placebo and 5.2% (n = 256) of those on fenofibrate had a coronary event (relative reduction of 11%; hazard ratio [HR ] 0.89, 95% CI 0.75-1.05; p = 0.16). This finding corresponds to a significant 24% reduction in non-fatal myocardial infarction (0.76, 0.62-0.94; p = 0.010) and a non-significant increase in coronary heart disease mortality (1.19, 0.90-1.57; p = 0.22). Totalicyclic disease events were significantly reduced from 13.9% to 12.5% ​​(0.89, 0.80-0.99; p = 0.035). This finding included a 21% reduction in coronary revascularisation (0.79, 0.68-0.93; 6.6% in the placebo group and 7.3% in the fenofibrate group (p = 0.18). Fenofibrate was associated with less albuminuria progression (p = 0.002), and less retinopathy needing laser treatment (5.2% vs 3.6%, p = 0.0003). There was a slight increase in pancreatitis (0.5% vs 0.8%, p = 0.031) and pulmonary embolism (0.7% vs 1.1%, p = 0.022) The primary outcome of coronary events. It did reduce total cardiovascular events, mainly due to fewer non-fatal myocardial infarctions and revascularisations. The higher rate of starting statin therapy in patients allocated placebo might have masked a moderately larger treatment benefit.