They showed that this treatment strategy caused cell cycle arrest at the G1 phase in female (HT-29) and male (SW480) colon cancer cells [35,66] by decreasing the expression of MYC [67,68], MYB, and the PROX1 [67] oncogenes and increasing the expression of the p21Waf1/Cip1 and p27Kip1 cell cycle inhibitors [35]. The gene discussed is PROX1; the disease is colonic neoplasm.