The anticancer activities of those strategies have occurred by regulating different genes and/or protein expression, including tumor suppressor genes such as p53 and Rb; oncogenes such as MYC, MYB, and PROX1; cell cycle regulators such as p21, p27, and cyclin A/D/E; caspase cascades such as caspase-9 and -3; migration-related factors such as uPA, uPA, MMP-2/9; and signaling pathways such as p38/MAPK, AKT, ERK1/2, JNK1/2, which are commonly linked with onset and progression of CRC. This evidence concerns the gene CDKN1A and colorectal carcinoma.