In arteriosclerosis, the released mtDNA forms a complex with the human antimicrobial peptide LL-37, which is resistant to degradation of deoxyribonuclease 2 and escapes autophagy recognition, leading to the activation of TLR9-mediated inflammatory response and the sustained activation of TLR9, causes autoimmune activation of chemokines and live cytokines, and exacerbates arteriosclerosis [19]. Here, CAMP is linked to arteriosclerosis disorder.