Of note, although we observed that Sox2+ cells in Ptch1−/−p53R172P lesions survived radiation and entered the cell cycle, the Sox2+ cells became a rare quiescent cell population in all recurrent SHH-MBs at end stages, comparable to untreated SHH-MBs (Figure 3F and G).20,21 In contrast, radiation treatment dramatically reduced tumor penetrance compared with untreated Ptch1+/−p53WT mice (38% to 9%), and tumor latency further increased by 29% in the only two treated mice (that still developed tumors) (Figure 3D). The gene discussed is SOX2; the disease is neoplasm.