These findings showed that NS398 influenced both GBM cell lines likewise, despite their different COX-2 expression levels, as well as the intrinsic genetic diversity, including TP53 gene status, MGMT activity, base excision repair (BER), or BRCA1 pathways, associated with their different TMZ-sensitivity/resistance [37,38,39]. This evidence concerns the gene PTGS2 and glioblastoma.