Recent studies revealed that the oncogenic pathway epidermal growth factor receptor (EGFR)/Phosphatidylinositol 3-Kinase (PI3K)/Protein kinase B (AKT) activates SREBP-1, that is directly involved in FA synthesis; indeed, SREBP-1 inactivation, through a pharmacological inhibitor or shRNA, reduces GBM proliferation in vitro and in vivo (Guo et al., 2009b; Geng et al., 2016). The gene discussed is AKT1; the disease is glioblastoma.