NFKB1 and neoplasm: Nevertheless, continual radiation activates NF-κB and then upregulates the expression of YY1 which could directly suppress miR-103a transcription, resulting in activating the DDR and promoting stemness and the expansion of tumor cells, thereby driving radioresistance and the recurrence of GBM [121].GBM is extremely heterogeneous and contains three subtypes, namely proneural (PN), mesenchymal (MES), and classical [122].