Mutual exclusivity analysis showed that mutations affecting B3GNT2, ST6GALNAC2, B4GALT2 individually, or any of the 36 candidate glycosylation genes as a group, as not being independent of known driver oncogenic mutations in KRAS or BRAF in colon cancer (Supplementary Table 4, Supplementary Fig. 1), indicating that the glycosylation defects may play a complementary role to other mitogenic signaling pathways in the multi-step colon cancer progression model. This evidence concerns the gene B3GNT2 and colonic neoplasm.