In LLD+/AF−, we found downregulated CCL3 and IL-18, both contributing to atherosclerosis, e.g., by inducing the recruitment of monocytes from the bloodstream to the vascular endothelium, causing the formation of foam cells, and promoting the retention and differentiation of leukocytes within the vascular endothelium or by proinflammatory effect [24,25]. The gene discussed is CCL3; the disease is atherosclerosis.