"Is the remarkable increase in HDL from CETP inhibitors the result of HDL "full dump trucks" getting backed-up in the system (and not flushing out through the liver as designed) as Dr. Wong once explained? I ask because at the end of the article a comment was made by John Maraganore; "R.I.P. HDL Hypothesis"" 

Yes, the dump truck analogy is a good one. Just because all your dump trucks are full to capacity doesn't mean that they are dumping their loads off to their destination. Instead of getting backed up, we want those trucks to be dumping off their contents, getting re-filled and repeating the process. The HDL hypothesis is not dead in my opinion. All the CETP inhibitor studies (anacetrapib, evacetrapib, dalcetrapib, torcetrapib) have shown is that perturbing with the CETP-mediated HDL remodeling step (#5 below) is not cardioprotective. 

HDL-cholesterol levels may be influenced at many steps:

1) rate of apolipoprotein AI (apoAI) synthesis and secretion (the major protein component of HDL);

2) rate of cellular cholesterol/phospholipid efflux to stabilize newly-secreted circulating apoAI and create stable, small HDL particles;

3) cellular cholesterol efflux to circulating small HDL particles that have a high capacity for uptake;

4) conversion of HDL "free cholesterol" to "cholesterol ester" by the action of the lipoprotein-bound enzyme LCAT (Lecithin–cholesterol acyltransferase). Conversion of free to esterified cholesterol makes the cholesterol less water soluble and moves the cholesterol to the central core of the HDL particle. Most of the cholesterol in the HDL particle is in the esterified form;

5) remodeling of HDL particles by the cholesterol ester transfer protein (CETP) enzyme, which catalyzes the reciprocal transfer of cholesterol ester (CE) from HDL for a triglyceride molecule from non-HDL lipoproteins (i.e. VLDL, LDL);

6) reverse cholesterol transport, which is the uptake of HDL-cholesterol from circulating HDL particles predominantly by the liver involving the scavenger receptor BI (SRBI).