Taking into account the already postulated relationship between atherosclerosis and AS37 based on histological findings that point to tissue mineralization, accumulation of lipids and inflammation38, the observed up-regulation of BGN in AS valves found in this work is in concordance with previous studies, and suggests this proteoglycan as an early initiator of the sclerotic lesion through an interaction with TLRs within the aortic valve. The gene discussed is BGN; the disease is aortic stenosis.