Altogether, we suggest that the “CKI bioactive compound (trifolirhizin, genistein-7-rutinoside, lanceolarin, and hesperetin-7-O-rutimoside)-target (mutant p53)-pathway (CHEK1-G2/M cell cycle arrest)” network is an important mechanism by which CKI prevents CRC. This evidence concerns the gene CHKA and colorectal carcinoma.