Further research into the functional consequences of HDAC1 knockdown in GBM cell lines revealed increased apoptosis and decreased cellular migration upon HDAC1 knockdown in vitro, alongside concomitant decreased levels of active AKT and ERK, highlighting a potential relationship between HDAC1 and the PI3K/AKT and Ras/ERK signaling pathways in GBM (53, 54). The gene discussed is AKT1; the disease is glioblastoma.