For downstream analyses, CNE-2 was excluded, as it has been reported to be contaminated with HeLa cells.15 To determine whether the sensitivity of cancerous cells to roniciclib might be influenced by the p53 tumor suppressor, which has previously been shown to intercede some of the antiproliferative and tumoricidal effects of CDK inhibitors,1,2 we also examined the viability of p53 wild-type (HCT-116-WT) and knockout (HCT-116-p53−/−) human colorectal cancer cell lines following roniciclib exposure. The gene discussed is TP53; the disease is colorectal cancer.