Preclinical studies, both in vitro and in vivo, consistently demonstrate that targeting Pyk2—particularly through the dual Pyk2/FAK inhibitors—can significantly suppress glioma invasion and proliferation, reduce tumor regrowth following surgical resection, and improve the cyto-toxic efficacy of TMZ, especially in TMZ-resistant or NF1-deficient tumors. Here, PTK2 is linked to neoplasm.