Knowing this and that (1) Brd4 is a necessary co-activator of iNOS transcription; (2) Brd4 is increasingly upregulated by photostress; (3) p65 is increasingly K310-acetylated by photostress; and (4) that the latter promotes Brd4 interaction with p65[59,63], we asked how the latter response might be suppressed in order to reduce iNOS upregulation in ALA/light-challenged glioblastoma cells. Here, BRD4 is linked to glioblastoma.