In fact, depending on the cellular context, p53 can modulate different tumor suppressor networks leading, for example, to induction of apoptosis, or inhibition of G1/S transition through the accumulation of p21, which in turn, inhibit the kinase activity of CDK2 and CDK4 in their cyclin complexes, or leading to the inhibition of G2/M transition through the decrease of Cyclin B1 levels [25–27]. The gene discussed is CDKN1A; the disease is neoplasm.