**3.4 Gene therapy**

Alghamri *et al.* recently published a thorough investigation of mutant versus wild-type IDH (wtIDH) gliomas in both murine and human models. Focusing on the murine data, the authors found wild-type IDH gliomas possessed more suppressive CD11b<sup>+</sup> Ly6G+ granulocytic MDSCs (gMDSCs) as well as increased PD-L1, iNOS, and Arg1 relative to gMDSCs derived from mutant IDH (mIDH) glioma bearing mice. Furthermore, murine mIDH glioma neurospheres were found to secrete significantly more G-CSF relative to their wtIDH counterparts. This increased secretion was determined to be caused by enrichment of H3K4me3 in the *Csf3* gene, which encodes G-CSF. Finally, when the immune-stimulatory gene therapy herpes simplex virus 1—thymidine kinase/Feline McDonough sarcoma (Fms)—like tyrosine kinase 3 ligand (TK/Flt3L) was used in combination with recombinant G-CSF (rG-CSF) in a wtIDH mouse model, a significant survival benefit was observed relative to TK/Ft3L or rG-CSF alone [147].
