This research shows recent genomic analyses have identified a distinct mutational signature in colorectal cancer (CRC) tissues linked to colibactin-producing E. coli (CoPEC) exposure, suggesting a direct role in driving tumorigenesis through mutations in key genes like APC and TP53.   Germline or somatic deficiencies in DNA crosslink repair pathways (e.g., FA, HR, MMR) increase susceptibility to colibactin by allowing its DNA lesions to be converted into fixed, oncogenic mutations rather than being properly repaired. The gene discussed is APC; the disease is colorectal cancer.