In this study, overexpression of PFKP was detected in human glioblastom﻿a (GBM) and resulted from AKT activation that, in turn, was induced by phosphatase and tensin homologue (PTEN) loss and epidermal growth factor receptor (EGFR)-dependent phosphoinositide 3-kinase (PI3K) activation. The gene discussed is AKT1; the disease is glioblastoma.