MKI67 and neoplasm: During the investigation of mice xenograft model, fluorescence images analysis and solid tumor weight measure results manifested that tumor growth in mice was memorably inhibited after knockdown of CCNI2. Downregulation of Ki‐67 expression levels detected by immunohistochemical staining suggested that the proliferation of CRC cells in the mice model was inhibited by knockdown of CCNI2. Based on the results of in vitro and in vivo experiments, we found that CCNI2 participated in the development of CRC by regulating the proliferation and apoptosis of CRC cells.