Consistent with those findings, our results indicated that inactivation of TLR9 downregulated MyD88, p-p65-NF-κB, and IRF7 and alleviated atherosclerosis progression, given that antibodies to RNA- or DNA-containing autoantigens are characteristic of systemic lupus erythematosus (SLE). The gene discussed is NFKB1; the disease is atherosclerosis.