However, studies of GOF mutp53-knockin mice, including R172H mutp53–knockin mice, showed that mutp53 accumulated specifically in tumors but not normal tissues, indicating that MDM2 can effectively degrade mutp53 in normal tissues but not in tumor tissues (41, 42), Furthermore, MDM2 deletion in R172H mutp53–knockin mice resulted in mutp53 accumulation in normal tissues, which in turn promoted tumor development and reduced mouse life span (24). Here, MDM2 is linked to neoplasm.