Purpose of Review <p>Cardiovascular disease (CVD) remains the leading global cause of death, with a significant proportion of events occurring despite optimal lipid-lowering therapy. This has shifted focus towards residual inflammatory risk, an emerging and modifiable target in atherosclerosis. This review explores inflammation’s central role in CVD, clarifies the role of high-sensitivity C-reactive protein (hsCRP) as a biomarker rather than a causal factor, and evaluates therapeutic advances in anti-inflammatory strategies.</p> Recent Findings <p>Clinical trials have demonstrated that inflammation is not merely a risk marker but a therapeutic target. Landmark studies including CANTOS and LoDoCo2 demonstrated a reduction in cardiovascular events following interleukin (IL)-1β inhibition and colchicine, respectively. The biomarker hsCRP remains a strong predictor of CV risk, although Mendelian randomization studies implicate the downstream cytokine IL-6, rather than CRP, as a more validated causal driver. Trials of IL-6 inhibitors and GLP1 receptor agonists suggest promise in broader cardiometabolic inflammation, with ongoing investigations across broad CVD conditions.</p> Summary <p>Inflammation is a validated and promising frontier in cardiovascular prevention. Translating these insights into practice will require refined biomarker-driven strategies, safe long-term agents, and interdisciplinary collaboration. Personalized targeting of residual inflammatory risk, with IL-6 emerging as a more validated therapeutic target compared to hsCRP, may significantly improve outcomes in complex, high-risk patients.</p>