Of note, our findings suggest that both GBM cell lines were equally influenced by NS398, despite the intrinsic diversity and individual genetic features, such as the TP53 gene status, MGMT activity and base excision repair (BER) or BRCA1 pathways, which in turn are associated to a different sensitivity or resistance to TMZ [55, 58, 59]. This evidence concerns the gene TP53 and glioblastoma.