NFKB1 and glioblastoma: Additionally, TTFields-treated RAW 264.7 cells displayed increased phosphorylation of IκB-α, the NF-κB p65 subunit and p38 MAPK.84 These data suggest that TTFields therapy mediates its antitumour immunity effects via the regulation of NF-κB and MAPK signalling pathways in RAW 264.7 macrophages, and raises the potential that TTFields could provide a way to overcome the mechanisms of immune escape typically associated with glioblastoma.87