Loss-of-function mutations in B3GALT5 and ST6GALNAC1 have been discovered in whole-exome sequencing studies of patients with IBD, and further studies of mice lacking the expression of B3GALT5 and ST6GALNAC6 (which encodes a protein similar in structure to ST6GALNAC1) decreases the sialylation of MUC2, a mucin implicated in the development of spontaneous colitis upon knockdown[79]. The gene discussed is MUC2; the disease is inflammatory bowel disease.