Previous studies have showed that dehydrocrenatidine induced cell cycle arrest in the G2/M phase, and inhibited the protein level of cyclin A, cyclin B, CDK2, CDK4, and CDK6 in oral cancer cells [34]; cell cycle arrest in the S and G2/M phases was also found in picrasidine I-treated oral cancer cells and led to apoptosis [20]; and picrasidine G increased the percentage of the sub-G1 phase in breast cancer [16]. Here, CCNA2 is linked to lip and oral cavity carcinoma.