Chronic inflammation is considered the basic pathomechanism of atherosclerotic diseases and a vast number of biomarkers and pathways were proposed to be involved in the process of atherosclerosis, such as tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and cluster differentiation 163 (CD163) and their soluble forms, sTWEAK and sCD163. This evidence concerns the gene CD163 and atherosclerosis.