Infection of cells with polyketide-peptide genotoxin (Colibactin) expressing E. coli led to a significant increase in frequency of gene mutation and anchorage-independent colony formation [50] Exposure of intestinal organoids to colibactin-producing E. coli led to mutational signature which is similar to mutational structure found in two independent CRC cohorts [51] Survival of cancer-associated E. coli intracellularly in macrophages led to persistent increase in COX-2 expression [52]. This evidence concerns the gene PTGS2 and cancer.