The eLDL (enzymatically modified LDL) hypothesis proposes that modification of LDL during atherogenesis occurs through the action of ubiquitous hydrolytic enzymes. eLDL is recognized by multiple macrophage receptors. Following cellular uptake, eLDL triggers atherosclerotic lesion initiation with reversion or progression depending on the balance between cholesterol insudation and depletion. The effects of eLDL on cellular constituents of the atherosclerotic lesion comprise both pro- and anti-inflammatory mechanisms. eLDL triggered complement activation is centrally involved in atherosclerosis with the first CRP (C-reactive protein)-dependent activation step to prevail at the early stages of atherogenesis (lesion initiation with reversion), and the second situation to gain dominance as local concentrations of eLDL surpass a critical threshold (lesion initiation with progression). Thus, CRP-mediated lipoprotein removal likely underlies the regression of early lesions, which occurs continuously through life. Perhaps CRP should be considered as an antiatherogenic agent and the question whether it is an innocent bystander or proatherogenic culprit is not really to the point. The observed association between CRP and atherosclerosis might simply be reverse causation: atherosclerotic disease progression induces CRP.