Human volunteer studies of V. cholerae mutants show that the clinical hallmarks of cholera require the combined production of two virulence determinants [14]: TCP, which is specified by the tcp operon and promotes small bowel colonization [15], and CT [16], which is encoded by the ctx operon and elicits a secretory response by small bowel epithelial cells. The gene discussed is SPINK1; the disease is vibrio infectious disease.