One potential chemotherapeutic agent for glioblastoma, sorafenib, is an oral multikinase inhibitor that blocks tumor cell proliferation and angiogenesis and induces tumor cell apoptosis by inhibiting serine/threonine kinases (c-RAF, and mutant and wild-type BRAF) and receptor tyrosine kinases, such as vascular endothelial growth factor receptors 2 and 3 (VEGFR2 and VEGFR3), platelet-derived growth factor receptor β (PDGFRβ), FLT3, and c-KIT [15]. This evidence concerns the gene MARK2 and neoplasm.