Thus, based on our data, we propose a model wherein DNA damage not only activates p53, but it also activates PITAR, with oncogenic properties, to inhibit p53-dependent functions, thus creating an incoherent feedforward mechanism to attenuate the response of p53 to DNA damage and promote oncogenesis and therapy resistance in GBM (Figure 8). Here, FAM95B1 is linked to glioblastoma.