According to many studies, low levels of high-density lipoprotein cholesterol (HDL-C) are an independent risk factor for coronary artery disease \[[@CIT0001]\].  HDL has several pleiotropic properties apart from reverse cholesterol transport; these include anti-oxidant, anti-inflammatory, anti-infectious, anti-proliferative, antithrombotic and vasodilator actions \[[@CIT0002]--[@CIT0004]\]. 

Randomised controlled trials, prospective and genetic studies, as well as meta-analyses have produced controversial results regarding treating low HDL-C levels \[[@CIT0005], [@CIT0006]\]. 

The functionality of HDL-C, as well as the role of dysfunctional HDL (dysHDL) in the prediction of cardiovascular (CV) risk has generated considerable debate.  Therefore, we read with interest the Dodani *et al*.  study \[[@CIT0007]\] which showed that dysHDL was significantly associated (*p* = 0.0024) with common carotid artery intima-media thickness (CCA-IMT) in 129 South Asian immigrants.  Chronic inflammation transforms HDL to dysHDL \[[@CIT0004]\].  However, the authors did not mention any correlation between high sensitivity C-reactive protein levels and the quantity of dysHDL or whether routinely measured HDL-C levels correlated with CCA-IMT and if any such relationship differs from dysHDL. 

It is apparent from the above, that not only the quantity, but also the quality of HDL matters (*Quantity and Quality; "Q and Q"*).  As a result, there is a need for new drugs that, apart from raising HDL-C levels, can improve HDL function \[[@CIT0008], [@CIT0009]\].  Cholesterol ester transfer protein (CETP) inhibitors (anacetrapib and evacetrapib) seem to be promising \[[@CIT0006]\].  However, there is no class effect, as the development of other CETP inhibitors (torcetrapib and dalcetrapib) was discontinued \[[@CIT0006]\]. 

It is worth emphasizing that we are at the beginning of dysHDL research.  Some issues need to be considered before confirming the potential predictive role of dysHDL \[[@CIT0004]\].  We need an easy and direct diagnostic method for dysHDL evaluation (possibly *via* measurement of highly specific microRNAs (miRs), as suggested in the DYS-HDL trial), as well as an optimal method for HDL subfraction analysis (to establish if certain subfractions are dysfunctional) \[[@CIT0002], [@CIT0010], [@CIT0011]\]. 

HDL carries specific miRs \[[@CIT0010], [@CIT0011]\].  Therefore, dysHDL-miRs, as well as HDL subfraction-miRs, could prove to be novel biomarkers of CV disease \[[@CIT0010], [@CIT0011]\].  Targeting HDL-miRs might also be a promising basis for drug development \[[@CIT0010], [@CIT0011]\].  It is crucial to identify the patients and conditions at the highest risk of dysHDL formation.  This population might benefit most from improving HDL "Q and Q" with a potential subsequent reduction in CV disease residual risk \[[@CIT0010]--[@CIT0013]\]. 

Conflict of interest {#S0001}
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This letter was written independently.  The authors did not receive financial or professional help with the preparation of the manuscript.  DPM has given talks, attended conferences and participated in studies sponsored by Merck, Sharp & Dohme (MSD) and Genzyme.  APA is supported by a grant from the Hellenic Atherosclerosis Society.  MB has given talks, attended conferences and participated in studies sponsored by Merck, Sharp & Dohme (MSD), Abbott, Sanofi and Amgen.  He is a member of the Amgen International Advisory Board.