Furthermore, in atherosclerosis, circ-SIRT1, derived from the SIRT1 gene, contributes to inhibiting NF-κB activation by direct interaction and promoting SIRT1 expression through competitively binding to miR-132/212 in vascular smooth muscle cells (82); however, AMPK signaling negatively regulates the NF-κB-TNFα inflammatory axis through increasing SIRT1 deacetylase activity and inhibiting NF-κB transcription activity by deacetylating p65, facilitating TNF-α signaling and triggering hepatic inflammation and fibrosis development (83). The gene discussed is NFKB1; the disease is inflammatory response.