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TP53 inactivation can occur by different mechanisms, such as MDM2/MDMX upregulation and downstream effects of NPM1 and FLT3 mutations; therefore, the targeting of these pathways is being investigated in the clinical setting. Blocking the MDM2-TP53 interaction with inhibitors, such as idasanutlin, KRT-232, or APG-115, can prevent the proteasomal degradation of TP53 and reinstate apoptosis mechanisms.