In addition, since SKP2 is overexpressed in several types of tumors and regulates the proteasomal stabilization/degradation of relevant proteins in glioma tumorigenesis, such as p21, myelocytomatosis (MYC) or cyclin D1, it could also be considered as a therapeutic target; several SKP2 inhibitors have been developed with beneficial effects in vitro and in vivo [42–45]. The gene discussed is MYC; the disease is glioma.