In addition to genetic mutations represented mainly as SNV and indels that have been encountered in the present investigation in key oncogene genes (such as TP73, PDE4DIP, FN1, KMT2C, MUC6, CREB3L1, GSE1, APC2, MUC16, and MLLT1) previous studies have elucidated that GBM was associated with alteration in other key signature oncogenes such as EGFR and PI3K, and that in over 40% of GBM carries one or more nonsynonymous mutation among the chromatin-modifier genes [37]. This evidence concerns the gene KMT2C and glioblastoma.