The PTEN-deficient tumor cells originally used in the findings described by Mendes-Pereira et al. (PTEN-/- HCT116: MLH1-deficiency) [32] and Shen et al. (PTEN-deficient PC3-AR: PARP1S383Y) [30] have since been shown to contain additional genetic lesions resulting in RAD51-independent HRD and enhanced cell sensitivity [83,84,85]. This evidence concerns the gene RAD51 and neoplasm.