The molecular mechanism of apigenin in cervical cancer treatment included down-regulated FAK signaling (FAK, paxillin, and integrin β1) and PI3K/AKT signaling (PI3K, AKT, and mTOR), which inactivated or activated various signaling targets, such as Bcl2, Bax, p21cip1, CDK1, CDC25c, cyclin B1, fibronectin, N-cadherin, vimentin, laminin, and E-cadherin, leading to mitochondrial-mediated apoptosis and G2/M-phase arrest, and reduced EMT to result in anticancer effects on cervical cancer (Figure 7). Here, CDKN1A is linked to cervical carcinoma.