Dyslipidemia stands as a significant risk factor for stroke, on par with the impact of hypertension, diabetes, and smoking. While the role of dyslipidemia is firmly established in the context of coronary artery disease, its influence on strokes remains somewhat enigmatic. This complexity likely arises from the diverse mechanisms underpinning strokes, which encompass a heterogeneous spectrum (hemorrhagic and ischemic; large artery atherosclerosis, small vessel occlusion, cardioembolism, and etc.). The extent to which lipid-lowering treatments affect stroke outcomes may vary depending on the specific stroke subtype. For instance, in cases of large artery atherosclerosis (LAA), the optimal target level of low-density lipoprotein cholesterol (LDL-C) is relatively clear. However, when dealing with other stroke subtypes like small vessel occlusion or cardioembolism, the appropriate LDL-C target remains uncertain. Furthermore, reperfusion therapy has emerged as the foremost treatment for acute ischemic stroke. Nevertheless, the precise relationship between LDL-C levels and outcomes in patients undergoing reperfusion therapy remains shrouded in uncertainty. Consequently, we have undertaken an in-depth exploration of the existing evidence supporting the utilization of lipid-lowering medications such as statins, ezetimibe, and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors. Our objective is to elucidate their role in secondary stroke prevention and the management of dyslipidemia across the various stroke subtypes.