It is remarkable that we continue to see challenges to the LDL hypothesis and that we also seem to need monographs defending it.1 How is it possible that we are still debating the empirical facts that low-density lipoprotein (LDL) cholesterol, or, more appropriately, apolipoprotein B–containing lipid particles, are the central actors in atherogenesis and that lowering LDL cholesterol with therapies that are proven safe and efficacious is one of our most effective strategies?