We found that primary GBM cells (Fig. 2g) or GBM cell lines (Fig. 2h), which lacked PTEN expression resulting from genetic deletions or mutations of PTEN, had higher levels of AKT phosphorylation and PFKP protein expression than did primary GBM cells, several GBM cell lines, or NHA with wild-type (WT) PTEN expression; of note, the levels of AKT phosphorylation were directly correlated with the PFKP protein expression levels. The gene discussed is PFKP; the disease is glioblastoma.