NFKB1 and colitis: Evidence showed that aberrant histone acetylation exists in UC patients (6) and colitis mice colon (31), while using histone deacetylase (HDAC) inhibitors could attenuate colitis by suppressing pro-inflammatory cytokines (32, 33), acetylating transcription of STAT1 and NF-κB (34, 35), increasing the formation of IL-35 via EBI3 (36), interacting with non-coding RNAs to fine-tune inflammatory responses (37), etc. Additionally, aberrant histone methylation patterns contribute to dysregulated inflammation (38, 39).