Gene-level analysis revealed that CNAmp of FANCM, the pivotal component of the Fanconi anemia (FA) pathway that relieves the DNA inter-strand cross-link 46, has significant correlations with cellular responses to DSB inducing agents such as topoisomerase inhibitor (camptothecin, P = 5.54×10-3), CHECK1/2 inhibitor (AZD7762, P = 1.90×10-5), and PARP inhibitors (olaparib: P = 3.34×10-3, veliparib: P = 1.29×10-4) (Table S4), which is consistent with previous studies showing that FANCM is intensively involved in the DDR response and regulates PARPi sensitivity 47,48. The gene discussed is PARP1; the disease is Friedreich ataxia.