TP53 and glioblastoma: More broadly across cancers, H2S exerts dose- and cellular condition-dependent effects on apoptosis: it can activate p53 and p38/MAPK signaling, increase ROS and sensitize glioblastoma lines to radiotherapy, or, conversely, bolster survival via NF-κB or PI3K/Akt pathways—implicating the quantitative and compartmental control of H2S/sulfane sulfur species as decisive for outcomes [45].