Although the functional consequences of this and most other ATM mutations is not known, given that in A–T many mutations in ATM induce protein truncation, protein destabilization and resulting loss of function [50], combined with the fact that siRNA-mediated loss of ATM in cancer cell lines results in PARP inhibitor sensitivity [30,31,32], it seems likely that many cancers with ATM mutation that lead to loss of function could be candidates for PARP inhibitor treatment. This evidence concerns the gene ATM and cancer.