Monocyte subsets are shifted towards the intermediate monocyte subtype in inflammation and reports about elevated CRP-levels in patients with degenerative AS suggest a regulation of monocyte subset distribution by inflammation.[35, 36] Though, we saw an increase in CRP-levels early after valve stenosis was treated with TAVR, which can be explained by inflammation due to post-interventional healing processes at the vascular access sites and within the left ventricular outflow tract. The gene discussed is CRP; the disease is aortic stenosis.