TP53 and cancer: 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).