In the attempt to define the role of PKM2 as a target of CPZ, we performed a further experimental set, in which U-87 MG and U-251 MG GBM cells, as well as RPE-1 non cancer cells, were assayed for glycoPER and OCR after PKM2 depletion via siRNA PKM2 silencing. The gene discussed is CPZ; the disease is glioblastoma.