Kdm6b, also known as JMJD3, is a histone demethylase that specifically removes methyl groups from H3K27me3, allowing re-expression of its target genes. This function is crucial in regulating gene expression and cell fate, playing roles in multiple biological processes such as development, differentiation, and disease-related pathways [4].

In osteosarcoma, Kdm6b is upregulated and promotes lung metastasis by mediating H3K27me3 demethylation of LDHA [1]. In glioblastoma, myeloid-specific deletion of Kdm6b enhances pro-inflammatory pathways and improves survival in tumor-bearing mice [2]. In cementoblasts, knockdown of Kdm6b inhibits HADHA-related fatty acid oxidation and mineralization [3]. In T-cell acute lymphoblastic leukemia (T-ALL), mouse cells deficient for Kdm6b cannot propagate T-ALL, and inactivating Kdm6b in human T-ALL patient cells leads to reduced cell survival [5].

In summary, Kdm6b is essential for regulating gene expression through histone demethylation. Studies using gene-knockout models in mice have revealed its significant roles in cancer metastasis, immune-related diseases, and tissue-specific cell functions such as cementogenesis. These findings suggest Kdm6b as a potential therapeutic target in relevant disease areas.