It can induce cell cycle arrest at different cell cycle phases, mainly at G0/G1 checkpoint via inhibiting the expression of cyclin D1 in different types of cancer cells by influencing of p53 [64–66] and regulates by increasing the expression of Cclk inhibitory proteins (Cdki), such as Cip1/p21 and Kip1/p27, inhibiting the expression of cyclin-dependent kinase (Cdk) 2, Cdk4, and Cdk6 and cyclins D1, D2, and E, as well as enhancing the binding of Cdki to Cdk [67, 68]. This evidence concerns the gene CCND1 and cancer.