are consistent with this, showing that the application of histone deacetylase (HDAC) inhibitor chidamide, and DNA damage agent etoposide to NKTCL cells not only played a synergistic role in anti-proliferation and enhanced apoptosis, but also made the cell cycle stop at the G2/M phase (58). This evidence concerns the gene HDAC9 and extranodal nasal NK/T cell lymphoma.