In addition to the abnormal activation of c-Met along with the progression of glioblastoma, liver [45], colon [46] and pancreatic [47] carcinomas, the selection of c-Met as a target protein for degradation is due to its deep involvement in the activation of several downstream signaling pathways (MAPK, PI3K, SRC, STAT) [48] that play an essential role in cell proliferation and survival. The gene discussed is MET; the disease is glioblastoma.