NFκB signals downstream of PI3K/AKT signalling, which is constitutively activated in many GBMs due to mutations in the tumour suppressor PTEN.5,6 NFκB binds the MGMT promoter at two sites and regulates its expression via p65 (RelA).7 Activation of NFκB is dependent on proteasomal activity, which catalyses the proteolysis of an inactive precursor into transcriptionally active p50/p65 subunits, as well as the destruction of the inhibitory factor IκBα.8,9 Thereafter, p65 translocates to the nucleus and MGMT is transcribed. Here, NFKB1 is linked to neoplasm.