At this point, Fur may be engaged to further activate the expression of TCP through binding and activation of the transcription of tcpP, toxT, and tcpA. While at HCD or at the later stage of infection (high number of V. cholerae cells in the intestine), high expressed HapR binds to the promoters of tcpP and tcpA to repress their transcription, and thus inhibits TCP and CT production, which then enables the pathogen to detach from the epithelium, and exits the host along with the stool. Here, FURIN is linked to infection.