In addition, disruptions in the transactivation capacity of p53 have been reported [141,142]; for instance, the nuclear protein Bcl2-like 12 (Bcl2L12), overexpressed in primary glioblastoma cells, binds to p53, inhibiting its transactivation potential, suppressing apoptosis via downregulation in the genic transcription of Bax, p21, phorbol-12-myristate-13-acetate-induced protein 1 (Noxa), and Puma [142], and contributing to therapeutic resistance in glioma cells. Here, BAX is linked to glioma.