Our in vitro studies showing enhanced ERK1/2 and AKT phosphorylation are corroborated by immunohistochemical data in tumor sections from GBM patients (Fig. 6a), also showing markedly stronger signals for HDAC6, EGFR, phosphorylated ERK1/2, and phosphorylated AKT compared to normal brain tissue (Fig. 6a). The gene discussed is AKT1; the disease is neoplasm.