Recently, it was reported that the introduction of a functional tcdC gene from a high toxin-producing strain that lacks any of the hyper virulence associated tcdC mutations (VPI10463, PCR ribotype 087) into an epidemic strain carrying a non-functional tcdC (M7404, PCR ribotype 027/NAP1/REA B1) can reduce toxin expression levels and moderately attenuate virulence [30] . This data seems consistent with the model discussed above. However, it is unclear how the levels of TcdC in the complemented strain relate to the physiological levels of the protein prior to the inactivation of TcdC in this strain background. The introduced tcdC gene, including its transcription signals, was derived from a different genetic background (VPI10463, Type 087) and was introduced on a multicopy plasmid. In addition, the reintroduction of TcdC in a strain lacking a functional TcdC, may affect processes that are not normally affected. Finally, the experiments were not corrected for the additional copies of the tcdC promoter that could result in the titration of regulators binding to those sequences.