As such, while in breast cancer models the presence of wild-type TP53 is a predictor of resistance to the use of PARPis [59], and the presence of mutations in the DNA-binding domain induces greater levels of PARylation and increased sensitivity to treatment with PARPi talazoparib [60], the same findings must not be extrapolated to models of lymphomas. This evidence concerns the gene TP53 and breast cancer.