The genomic signatures were similar in the two components and both harbored identical mutations in PTEN, RB1, TERT promoter, and TP53. However, compared to the glioblastoma background, the epithelioid component possessed additional copy number alterations as well as different and unique immune cells infiltration by CD4+ lymphocytes and NK cells, strongly supporting the hypothesis that the epithelioid component of the tumor evolved from a background of glioblastoma and could have been arisen by increased tumor instability or selected by specific tumor microenvironment niche. This evidence concerns the gene RB1 and neoplasm.