They hypothesized that KIF18B may function through Wnt/β-catenin pathway and verified the down-regulation of C-myc, β-catenin, and phosphorylated GSK3β after the knockdown of KIF18B. Moreover, the volumes and weight of the tumor were obviously reduced in mouse model after down-regulation treatment of KIF18B. The results have uncovered that KIF18B acts as a potential oncogene in cervical cancer. This evidence concerns the gene MYC and cervical carcinoma.