For example, epigenetic silencing of the NY-ESO1 gene in glioma and mesothelioma cells required the sequential recruitment of three independent complexes: (i) HDAC1/mSIN3a/NCOR complex which deacetylates the promoter, (ii) DNMT3B/HDAC1/EGR1 complex which induces a local DNA methylation and increases histone deacetylation, and (iii) DNMT1/PCNA/UHRF1/G9a complex which maintains DNA methylation and introduces the H3K9me2 repressive mark [164]. The gene discussed is DNMT1; the disease is glioma.