This essay provides a comprehensive overview of atherosclerosis, framing it as an inflammatory disease primarily resulting from high plasma cholesterol concentrations. It delves into the pathophysiology of the disease, highlighting the role of endothelial dysfunction, modified lipoproteins like LDL, and the inflammatory responses involving macrophages and lymphocytes. The paper references experimental and patient-based studies that validate Russell Ross's proposition regarding atherosclerosis, including the impact of hypercholesterolemia, modified lipids, and homocysteine. Furthermore, it explores cellular interactions and the influence of blood flow on lesion development, emphasizing the cyclic nature of rupturing and healing in arteries. The essay concludes by acknowledging advancements in genetic technologies and animal models used in atherosclerosis research, suggesting that selectively modifying harmful inflammatory components could lead to improved diagnostic and management strategies.