MCF10A breast epithelial cells with low Cdk2 entered a transient G0-like state in which they were sensitive to arrest by an inhibitor of MEK (a mitogen-stimulated kinase), whereas those with residual Cdk2 were refractory to MEK inhibition, retained detectable Rb phosphorylation (albeit on a site that was refractory to allele-specific inhibition of Cdk2 in human colon cancer-derived cells19—see below), and could commit to another round of division immediately. Here, MAP2K7 is linked to colonic neoplasm.