Interestingly, high expression of LL-37 has been reported in atherosclerotic lesions vs. healthy vascular tissue [17], and furthermore, Lundberg et al. [29] have reported that deleting TLR3 in immune cells attenuates both aortic inflammation and atherosclerosis in mice, suggesting that LL-37-induced potentiation of TLR3 signaling indeed can be of pathophysiological importance. The gene discussed is TLR3; the disease is atherosclerosis.