SOCS1 and SOCS3 mediate degradation of the NF-κB family member p65/RelA, focal adhesion kinase (FAK), von Hippel Lindau (vHL), Janus kinase 2 (JAK2) and indoleamine 2,3-dioxygenase (IDO), all of which play essential roles in GBM progression and chemo-/radioresistance (Table 1) [24–28]. The gene discussed is PTK2; the disease is glioblastoma.