Interestingly, in most cases of MIN pathway cancers these frameshift mutations were biallelic or homozygous/hemizygous, indicating that PRDM2 follows the two-hit model of tumor suppressor genes, with one hit achieved either by mutations/deletions affecting the PR domain or by frameshift mutations in the 3′ end affecting the interactions between the N-terminal PR domain of RIZ1 and its C-terminal region, including the PR-binding motif [59]. Here, PRDM2 is linked to neoplasm.