1. Adv with E1B and E1A mutations target defects in p53 or Rb pathways of tumor cells 2. RGD or EGFR modification retargets GBM cells with low CAR expression 3. The anti-tumor effect in vivo mainly depends on oncolysis and the changes in the GBM microenvironment mediated by T cells and macrophages. Here, DHTKD1 is linked to glioblastoma.