To further verify our assumption, we used two KRAS-mutant human colon cancer cell lines: HCT-116 cells, which have wild-type p53 (p53+/+) and a subline that is deficient in p53 (HCT-116 p53−/−), to explore whether p21 activation was mediated by p53 in response to BI-2536/fasudil. The gene discussed is CDKN1A; the disease is colonic neoplasm.