Some in vitro experimental results can explain the above phenomenon: (1) The occurrence of KRAS mutations may cause excessive cell proliferation; (2) This hyperproliferation signal is a stress signal, which can trigger the release of wild p53 from mice mdm2; (3) the released wild p53 can stop the cell cycle, initiate the apoptosis program, and protect the cells from abnormal growth factors (Suh et al., 2011); and (4) The mutant p53 lost its original tumor suppressive function and cooperated with the KRAS mutant gene to promote cancer progression (McMurray et al., 2008). The gene discussed is TP53; the disease is neoplasm.