Indeed, Ca9-22 cells treated with 5 μM showed a cell-cycle arrest, by increasing the expression of cyclin-dependent kinase inhibitors (CDKIs) such as p21, p27, p16 or p53 and Rb (retinoblastoma protein) which are tumor suppressor genes known to be inactive in most cancer types, while it inhibits oncogenes such as cyclin D1 or c-Myc. The gene discussed is TP53; the disease is cancer.