For instance, PTPRZ1 is considered as an oncogene for promoting tumor growth in glioma that further results in the malignant progression of glioma by fusion with MET proto-oncogene, receptor tyrosine kinase (MET) [10]; in breast cancer, PTPRZ1 reduces the chemosensitivity through promoting tumor cell growth and suppressing cell apoptosis [11]; the proliferation of renal cell carcinoma (RCC) cells enhanced by PTPRZ1 is dependent on the inactivation of von Hippel-Lindau tumor suppressor (VHL), while PTPRZ1/β-catenin pathway may be a potential target for the treatment of non-active VHL RCC [12]. This evidence concerns the gene MET and central nervous system cancer.