For example, p65 O-GlcNAcylation enhances NF-κB activation by decreasing its binding to IκB-α (Yang et al., 2008); on the contrary, sirtuin 1-mediated p65 deacetylation at a lysine site (Lys310) suppresses NF-κB transcriptional activity (Planavila et al., 2011), thereby modulating cardiac inflammation. This evidence concerns the gene NFKB1 and inflammatory response.