Many available studies examining replication stress to date have focused on individual tumor types, for example in ovarian cancer (74), pancreatic cancer (75, 76), or selected features that drive replication stress, for example overexpression of oncogenes (via overexpression of CDC25A, CCNE1 or MYC; ref. 77) or replication stress response defects (via depletion of ATR, ATM, CHEK1, or CHEK2; ref. 44). This evidence concerns the gene CDC25A and familial pancreatic carcinoma.