The role of Tir8/Sigirr was recently investigated in the Apcmin/+ model, a spontaneous intestinal cancer model mimicking the Familial Adenomatous Polyposis syndrome, where loss of heterozygosity (LOH) of the tumor suppressor Apc is the exclusive genetic alteration leading to the tumor initiation in the Apcmin/+ mouse (Yamada et al., 2002). This evidence concerns the gene SIGIRR and neoplasm.