In addition to our study, other mechanism-specific CNA profiles are emerging: Array CGH and single-cell sequencing of tumors formed in mouse models of deregulated Mre11 (DNA double-strand break repair factor) and the DNA replication licensing factor MCM2 revealed distinctive CNA landscapes biased towards small deletions, although these were necessarily the product of both mutation and selection during tumor evolution [55, 56]. Here, MRE11 is linked to neoplasm.