For instance, colibactin producing E. coli species have recently been shown to induce distinct mutational signatures associated with CRC, using luminal injection techniques with intestinal organoid models.4 It remains to be shown whether and how Fn interacts with CRC cells in detail, yet the present work by Zepeda-Rivera et al. allows future mechanistic studies to focus on the Fna C2 clade as the highly prevalent and virulent subgroup of Fn in CRC. The gene discussed is FN1; the disease is colorectal carcinoma.