While early work revealed that RUNX3 inhibits cancer initiation by inhibiting cell cycle entry and inducing apoptosis [47,48], it is tempting to hypothesize that one of RUNX3’s tumor suppressor properties may reside in its function as a reprogramming barrier or through maintenance of a stable differentiated state and that Runx3 inactivation correlates with increased plasticity and/or the acquisition of a stem-cell-like state. The gene discussed is RUNX3; the disease is neoplasm.