For instance, the activation of oncogenes within cells may trigger a state known as oncogene‐induced senescence (OIS), in which cells enter an irreversible state of growth arrest, thus preventing the formation of tumors.[40, 41] Consistent with our findings, B68 significantly upregulated the expression of p21 and p53 when acting on colorectal cancer cells, whereas B68 treatment significantly increased the percentage of β‐gal‐positive senescent cells in tumor tissue, causing cycle arrest. Here, TP53 is linked to neoplasm.