The CRISPR and pharmacological sensitivities are consistent with attenuated TP53 activity resulting from inhibitions by MDM2. We hypothesized that pharmacological MDM2 inhibition would reactivate wildtype TP53, and so cause a shift from neutral to positive fitness in TP53. To test this, we carried out in vivo assays using the signaling library with mice randomized to receive 100 mg/kg Idasanutlin or vehicle control for 14 days, starting from a small tumour size of ~0.05 cm3. Here, MDM2 is linked to neoplasm.