In adenomyosis, the NF-κB pathway is in a state of abnormal activation, which is mainly caused by factors such as TNF-α, IL-1β, LPS, etc. Subsequently, IKKα and IKKβ phosphorylate IκBα, leading to its ubiquitination and proteasome-mediated degradation, thereby releasing p50/RelA as a transcription factor to activate the transcription of target genes (Guo et al., 2024). This evidence concerns the gene NFKB1 and adenomyosis.