Together, our analysis demonstrates that the simultaneous perturbation of MYB, HDAC2, and FOXA2 has the most pronounced influence on controlling the Boolean GRN model toward the desired state and that the states of the downstream nodes canalized by the control of MYB, HDAC2, and FOXA2 in simulation analysis largely agree with the results of in vitro knockdown experiments on the colorectal cancer cells. The gene discussed is HDAC2; the disease is colorectal cancer.