For example, germline or somatic mutations in one of the DNA damage repair genes ATM, BRCA1, BRCA2 or PALB2 could potentially sensitise these tumours to platinum-based chemotherapy or poly-(ADP-ribose) polymerase inhibition.65 In addition, there is a low prevalence of alterations in several genes that are potentially amenable to other targeted therapies, including BRAF, PIK3CA, RNF43, STK11 and JAK1, as well as focal high-level amplifications in ERBB2. 7 This evidence concerns the gene ATM and neoplasm.