An increased frequency of intestinal tumors was observed in Mbd4−/−Apcmin/+ mice, showing increased CpG to TpG mutations in the Apc gene (36, 131), although it must be noted that in the Wong et al. (131) study the Mbd4 exon 3 deletion mutant mouse strain was used, which potentially has retained glycosylase activity (124), raising some doubts on the involvement of MBD4 as a glycosylase in these studies. Here, MBD4 is linked to intestinal neoplasm.