Despite previous experimental evidence that, dissociation of the pentameric CRP may contribute to inflammation and atherosclerosis via pro-inflammatory effects of monomeric CRP [33], our current findings are in agreement with recent human genetic data indicating that CRP itself is highly unlikely to be even a modest causal factor in CAD [34] and with the general notion of limited value of this marker for individual clinical risk profiling [35], [36]. The gene discussed is CRP; the disease is atherosclerosis.