Excessive EZH2 activity leads to elevated H3K27me3 levels, causing a shift in the lineage commitment of BMMSCs toward adipocytes during osteoporosis.76 Further investigations reveal significant enrichment of both EZH2 and H3K27me3 in the promoters of Wnt1, Wnt6, and Wnt10a within BMMSCs of mice subjected to ovariectomy.77,78 Notably, EZH2 reduces the enrichment of H3K27me3 on these promoters, consequently suppressing the expression of Wnt genes. The gene discussed is EZH2; the disease is osteoporosis.