Li et al. [76] showed that GBM (glioblastoma multiforme) cell-derived ExVs containing programmed cell death 1 (PD1) contributed to the modulation of LRRC4 on T cells, whereby miR-101 reversed the promoter hypermethylation and induced the re-expression of LRRC4 in GBM cells by targeting the histone methyltransferase enhancer of zeste homolog 2 (EZH2), the EZH2 cofactor embryonic ectoderm development (EED) and DNA methyltransferase 3A (DNMT3A). The gene discussed is LRRC4; the disease is glioblastoma.