Magatti et al. (2012) demonstrated that hAM-derived cells downregulate the expression of cyclins D2, E1, and H and cyclin-dependent kinases (CDK4, CDK6, and CDK2) and upregulate the negative regulators of cell cycle, such as p15 and p21 (Magatti et al., 2012). Furthermore, Riedel et al. (2019) showed that the conditioned medium of hAM induces cell cycle arrest in the HepG2 human liver cancer cell line in the G2/M phase (Riedel et al., 2019), which further supports our hypothesis that hAM homogenate affects multiple targets in the cell cycle of cancer cells. This evidence concerns the gene CDK4 and cancer.