We then used a combination of DNA maintenance, replication, and cell cycle regulation network–related transcriptional profiles from GO and pathway enrichment analysis to define replication stress using mechanisms associated with DNA replication (ATR activation, chromosomal maintenance, E2F transcriptional pathways, HR, Fanconi anemia, base-excision repair, p53 signaling, endoplasmic reticulum stress, and RNA processing). Here, TP53 is linked to Fanconi anemia.