Atherosclerosis is increasingly recognized as a chronic inflammatory disease rather than a purely lipid-storage disorder. Its pathogenesis begins with endothelial dysfunction, which disrupts vascular homeostasis and promotes the retention and modification of apolipoprotein B-containing lipoproteins within the arterial wall. These altered lipoproteins trigger an inflammatory response that recruits monocytes, which differentiate into macrophages and become foam cells, contributing to fatty streak formation and plaque development. As the lesion progresses, activation of innate immunity, particularly through the NLRP3 inflammasome, amplifies the production of inflammatory mediators such as interleukin-1 beta, interleukin-6, tumor necrosis factor-alpha, and C-reactive protein, thereby promoting plaque instability and thrombotic complications. Although statins remain central to atherosclerosis management because of their lipid-lowering and pleiotropic anti-inflammatory effects, they do not fully eliminate residual inflammatory risk, which has emerged as a strong predictor of recurrent cardiovascular events. This has led to growing interest in targeted anti-inflammatory therapies that address specific inflammatory pathways involved in disease progression. Canakinumab and colchicine have demonstrated that selective modulation of inflammation can reduce major adverse cardiovascular events, whereas neutral trials such as CIRT have highlighted the importance of pathway specificity. Emerging therapies, including interleukin-6 inhibitors, NLRP3 inflammasome inhibitors, pro-resolving mediators, nanoparticle-based delivery systems, and gene-based approaches, offer promising directions for future treatment. However, optimal implementation requires careful patient selection, biomarker integration, imaging-based risk assessment, and a precision medicine approach that balances efficacy, safety, and cost while complementing intensive lipid-lowering strategies.