Statins remain the cornerstone of hypolipidaemic drug treatment. The recent 
American College of Cardiology (ACC)/American Heart Association (AHA) lipid 
guidelines suggest using percent reductions of low density lipoprotein 
cholesterol (LDL-C), according to cardiovascular disease (CVD) risk, rather than 
specific LDL-C targets. These guidelines raised concerns and other Societies 
(US, International, European) have not endorsed them. The implementation of 
previous guidelines in clinical practice is suboptimal due to attitudes of 
physicians and restrictions in health care systems. Monoclonal antibodies that 
inhibit proprotein convertase subtilisin/ kexin type 9 (PCSK9), which degrades 
the LDL receptor, like alirocumab and evolocumab, are in phase 3 trials. These 
drugs are suitable for statin intolerant or resistant patients, heterozygous 
familial hypercholesterolaemia (HeFH) and some forms of homozygous FH (HoFH). 
Mipomersen (antisense oligonucleotide against apolipoprotein B) and lomitapide 
(microsomal triglyceride transfer protein blocker) have already been approved 
for HoFH. Eventually, silencing micro-RNA oligonucleotides may also become 
available. The repair or silencing of genes implicated in hyperlipidaemia and/or 
atherosclerosis is also on the horizon. If the new therapeutic options mentioned 
above prove to be effective and safe then by combining them with statins and/or 
ezetimibe we should be able to effectively control acquired or hereditary 
dyslipidaemias and substantially further reduce CVD morbidity and mortality.