Genetic analysis of the available tumor baseline biopsies indicated that all tumors harbored wild-type TP53. Interestingly, genetic analysis of cell-free DNA in plasma samples of these patients showed the appearance of TP53 mutations upon treatment with the HDM2 antagonist, indicating a possible mechanism of required resistance to HDM2 inhibition, and most probably explaining the observed limited activity [22]. Here, TP53 is linked to neoplasm.