Double-stranded RNA can be released from damaged/stressed cells in diseased aortic valves, and endogenous TLR3 activation can contribute to experimental aortic valve stenosis.16 These findings underscore the potential significance of our finding that in patient with TAVS, circulating monocytes are primed to a hyperresponsiveness to TLR3 stimulation. This evidence concerns the gene TLR3 and stricture.