Cardiometabolic risk factors such as hyperlipidaemia, diabetes, hypertension, smoking, unhealthy diet, and sedentarism contribute to inflammation in the vascular wall, fibrous cap formation, and eventually rupture of the atherosclerotic plaque. Alterations in metabolic enzymes carry the potential to influence plaque progression (pro-atherogenic) or stabilisation (anti-inflammatory), becoming potential targets for immunometabolic modulation in atherosclerosis. Bottom panel highlights major mechanisms associated with different metabolic enzymes. Abbreviations: ARG1, arginase 1; FAS, fatty acid synthase; GLUT1, glucose transporter 1; HIF-1a, hypoxia inducible factor 1α; KYAT, kynurenine oxoglutarate transaminase; SGLT2, sodium-glucose cotransporter-2.