Dyslipoproteinemias such as elevated LDL-cholesterol, reduced HDL-cholesterol, elevated triglycerides and elevated lipoprotein(a) play a central role in atherosclerosis. An elevated LDL concentration is pro-atherogenic because LDL are intimately linked to oxidative and inflammatory processes in the arterial wall. HDL on the other hand are anti-atherogenic because they mediate cholesterol efflux from the arterial wall, modulate the metabolism of atherogenic lipoproteins, and directly affect endothelial function. The current therapeutic focus is on LDL reduction and much less on HDL elevation, although fibrates and particularly nicotinic-acid/niacin are potent drugs to increase HDL-cholesterol and although both groups of drugs have been proven beneficial in large end-point studies. Furthermore, new HDL raising drugs are being developed. In patients with established atherosclerosis or at high risk for atherosclerosis statin-based LDL reduction will remain the cornerstone of lipid therapy, but many patients may benefit from combination therapy aiming at optimizing all lipid parameters.