Some doctors and researchers believe the benefit from statins is more to do with the decrease in inflammation caused by them. Possibly widespread use of statins has beneficial effects on other disease processes too.
https://en.wikipedia.org/wiki/CETP_inhibitor
Anacetrapib is still in stage III trials so it's too early to consider the concept a failure, but I think the bad results so far are evidence that hyperlipidemia is a symptom not a cause of cardiovascular disease, and that statins have some mechanism of action beyond just modifying cholesterol levels (eg. anti-inflammatory, as some people have suggested).
AKA
Cause A results in hyperlipidemia.
Cause B results in hyperlipidemia.
Cause C results in hyperlipidemia and arterial plaques.
Cause D results in hyperlipidemia.
Multiple agents that reduce cholesterol, including ezetemibe and statins, reduce cardiovascular disease outcomes and death.
Multiple cholesterol-related genes, including HMGCR, LDLR, APOB, PCSK9, and ANGPTL3, contain variants which influence both LDL cholesterol and the risk for coronary artery disease, myocardial infarction, and death.
And Mendelian randomization studies that rely upon a dose-response relationship between genes that influence cholesterol and the cardiovascular outcomes that they cause have also demonstrated a link between genetically driven cholesterol levels and hard endpoints.
So, one set of drugs (CETP inhibitors) that don't seem to follow the story are more likely to be the exception, rather than the rule. Interesting biology awaits us in the explanation of why the CETP inhibitors don't do what we imagined they would with hard outcomes.
Only in small selected populations.