Disease progression occurred significantly earlier on ATM-mutated patients.59 These findings have later been confirmed in clinical trials as ATM-deficient tumours have consistently shown limited response to different PARPi.19,54,57,58 Similar lack of response has been seen in patients with CDK12 inactivation.19,54,57,58 On the contrary, promising results have been observed for patients with alterations in PALB2, BRIP1, FANCA or RAD51B. 58 However, due to the low prevalence of these aberrations, further data are needed to fully understand their value as predictors of response to PARPi. The gene discussed is ATM; the disease is neoplasm.