Epigenetic dysregulation, including heightened HDAC activity, is a hallmark of GBM [55,57] .In this context, THOC1-dependent recruitment of SIN3A–HDAC1/2 is predicted to exert stronger deacetylating and chromatin-compacting effects at target loci, thereby limiting R-loop accumulation and DNA damage. This evidence concerns the gene HDAC1 and glioblastoma.