[[Kinesin]] superfamily protein 4 (KIF4), a KIF member classified in [[Kinesin]] 4 has been indicated as a mediator acted in the [[tumorigenesis]] of human [[cancer]]. The mechanism of [[KIF4A]] in [[glioma]] is yet to be investigated. 
Zhang et al. explored the potential function and mechanism of KIF4A in gliomas. 
They analyzed the KIF4A expression and the prognosis in glioma patients using [[The Cancer Genome Atlas]] (TCGA) databases. KIF4A levels in normal human [[astrocyte]] cell (NHA) and glioma cell lines were examined by [[Western blot]]. They studied the function of KIF4A on proliferation, migration, invasion, and cell cycle in glioma cell lines using a series of in vitro and in vivo experiments. Chromatin Immunoprecipitation (ChIP) analysis was applied to search potential KIF4A related downstream in glioma. 
They identified the significantly up-regulated expression of KIF4A both in glioma tissues and cells. Glioma patients with elevated KIF4A expression have shorter survival. Down-regulation of KIF4A exerted an inhibitory effect on cell proliferation, invasion, and migration. We crucially identified that KIF4A drives glioma growth by transcriptional repression of Rac1/Cdc42 to induce cytoskeletal remodeling in [[glioma cell]]s. [[Knockdown]] of KIF4A decreased [[RohA]], [[Rac1]], [[Cdc42]], [[Pak1]] and [[Pak2]] expression level. The study provided a prospect that KIF4A functions as an [[oncogene]] in glioma
((Zhang H, Meng S, Chu K, Chu S, Fan YC, Bai J, Yu ZQ. KIF4A drives glioma growth by transcriptional repression of Rac1/Cdc42 to induce cytoskeletal remodeling in glioma cells. J Cancer. 2022 Nov 21;13(15):3640-3651. doi: 10.7150/jca.77238. PMID: 36606197; PMCID: PMC9809311.)).