From adenoma (a network carrying a mutation in APC) to the late adenocarcinoma stage (a network with mutations in APC, KRAS, and PTEN), we found that it is possible to drive all initial states of the attractor landscape into the attractor of a normal proliferative phenotype by changing the status of four target nodes, beta-arrestin, P115RhoGEF, Smad2/4, and ERK. This evidence concerns the gene KRAS and adenocarcinoma.