Altered HDAC functions have also been confirmed in GBM, leading to the upregulation of receptor tyrosine kinase (RTK)/Ras/phosphoinositide-3-kinase (PI3K), p53, retinoblastoma (Rb), EGFR, and phosphatase and tensin homolog (PTEN) signaling pathways [90]. This evidence concerns the gene EGFR and glioblastoma.