The role of human endogenous retrovirus K (HERV-K, HML-2) in glioblastoma has been experimentally demonstrated: CRISPR interference targeting HML-2 LTR5Hs elements in patient-derived glioblastoma neurospheres led to marked reductions in neurosphere formation, OCT4 and Nestin expression, and tumorigenicity in intracranial xenografts, resulting in prolonged survival. Here, POU5F1 is linked to glioblastoma.