The initially impressive response to BEV treatment in GBM patients, dubbed as “pseudo response” due the subsequent relapse of the tumor, often in a more invasive form, was thought to be resulting from the manifestation of an initial “normalization” of perfusion that increases hypoxia, both increasing apoptosis as well as upregulating the H1F1 axis. This evidence concerns the gene H1-1 and glioblastoma.