Numerous other mechanisms are suggested to contribute to aberrant NF-κB signalling in GBM, including NF-κB activation by peptidyl-prolyl isomerase PIN1, mixed lineage kinase 4 (MLK4), heterozygous deletion of NFKBIA, the gene encoding IκBα, high levels of micro(mi)RNA-30e*, which targets IκBα, as well as DNA-damage [41,42,43,44,45]. Here, PIN1 is linked to glioblastoma.