Concerning GBM, it has been shown that the HDAC functions are also altered and determine the abnormal activation of receptor tyrosine kinase (RTK)/Ras/phosphoinositide-3-kinase (PI3K), p53, retinoblastoma (Rb), epidermal growth factor receptor (EGFR), and phosphatase and tensin homolog (PTEN) signaling pathways [30]. Here, HDAC9 is linked to glioblastoma.