Data from mouse models of colon cancer suggest that resistance to Gemcitabine may be the result of increased metabolic degradation of Gemcitabine into difluorodeoxyuridine by the long isoform of the bacterial enzyme cytidine deaminase (CDDL), mainly found in the γ-amastigotes phylum (Geller et al., 2017; Choy et al., 2018). Here, CDA is linked to colonic neoplasm.