Dyslipidemia is a major risk factor for atherosclerotic cardiovascular disease (ASCVD). Current guidelines focus on lowering low-density lipoprotein cholesterol (LDL-C) with statins, which remain the first-line therapy for secondary prevention of atherosclerotic disease and primary prevention in high-risk patients. However, statins are insufficient for preventing acute myocardial infarction in primary or secondary prevention. Emerging therapies, including genetic therapies, RNA-based treatments, and nanotechnology, are being explored to improve cardiovascular outcomes. This review summarizes current and emerging therapies for dyslipidemia management. Statins reduce LDL-C by inhibiting HMG-CoA reductase, increasing LDL receptors, and lowering LDL-C levels. They also have modest effects on triglycerides and HDL-C. Statins are effective in primary and secondary prevention, with studies showing reduced cardiovascular events in high-risk patients. However, their benefits in low-risk populations are limited, and NNTs are high. Statins are also beneficial in special groups, such as patients with diabetes, chronic kidney disease, heart failure, and HIV, though some studies show limited efficacy in dialysis patients. PCSK9 inhibitors, such as alirocumab and evolocumab, significantly lower LDL-C by increasing LDL receptors. They also reduce Lp(a) levels and have shown benefits in reducing cardiovascular events. However, their effectiveness is limited in patients with homozygous familial hypercholesterolemia. Tafolecimab and lerodalcibep are new PCSK9 inhibitors with promising results. Ezetimibe reduces cholesterol absorption by inhibiting NPC1L1, leading to lower LDL-C levels. It is effective in combination with statins but has limited benefits in patients with very low LDL-C. Bempedoic acid, an ACL inhibitor, also lowers LDL-C and is effective in statin-intolerant patients. Lp(a)-targeted therapies are still under development, though some drugs like PCSK9 inhibitors and mipomersen can reduce Lp(a) levels. Bile acid-binding resins reduce LDL-C by binding bile acids and increasing cholesterol excretion, but they have limited efficacy and gastrointestinal side effects. Niacin increases HDL-C and reduces triglycerides but has side effects and is less effective in combination with statins. Fibrates reduce triglycerides and increase HDL-C but have limited benefits in primary prevention and are not recommended for cardiovascular prevention due to lack of evidence. This review highlights the importance of individualized treatment strategies for dyslipidemia, considering patient risk factors and the potential benefits of emerging therapies.Dyslipidemia is a major risk factor for atherosclerotic cardiovascular disease (ASCVD). Current guidelines focus on lowering low-density lipoprotein cholesterol (LDL-C) with statins, which remain the first-line therapy for secondary prevention of atherosclerotic disease and primary prevention in high-risk patients. However, statins are insufficient for preventing acute myocardial infarction in primary or secondary prevention. Emerging therapies, including genetic therapies, RNA-based treatments, and nanotechnology, are being explored to improve cardiovascular outcomes. This review summarizes current and emerging therapies for dyslipidemia management. Statins reduce LDL-C by inhibiting HMG-CoA reductase, increasing LDL receptors, and lowering LDL-C levels. They also have modest effects on triglycerides and HDL-C. Statins are effective in primary and secondary prevention, with studies showing reduced cardiovascular events in high-risk patients. However, their benefits in low-risk populations are limited, and NNTs are high. Statins are also beneficial in special groups, such as patients with diabetes, chronic kidney disease, heart failure, and HIV, though some studies show limited efficacy in dialysis patients. PCSK9 inhibitors, such as alirocumab and evolocumab, significantly lower LDL-C by increasing LDL receptors. They also reduce Lp(a) levels and have shown benefits in reducing cardiovascular events. However, their effectiveness is limited in patients with homozygous familial hypercholesterolemia. Tafolecimab and lerodalcibep are new PCSK9 inhibitors with promising results. Ezetimibe reduces cholesterol absorption by inhibiting NPC1L1, leading to lower LDL-C levels. It is effective in combination with statins but has limited benefits in patients with very low LDL-C. Bempedoic acid, an ACL inhibitor, also lowers LDL-C and is effective in statin-intolerant patients. Lp(a)-targeted therapies are still under development, though some drugs like PCSK9 inhibitors and mipomersen can reduce Lp(a) levels. Bile acid-binding resins reduce LDL-C by binding bile acids and increasing cholesterol excretion, but they have limited efficacy and gastrointestinal side effects. Niacin increases HDL-C and reduces triglycerides but has side effects and is less effective in combination with statins. Fibrates reduce triglycerides and increase HDL-C but have limited benefits in primary prevention and are not recommended for cardiovascular prevention due to lack of evidence. This review highlights the importance of individualized treatment strategies for dyslipidemia, considering patient risk factors and the potential benefits of emerging therapies.