Mice haploinsufficient for Atad5(Atad5+/m) display high levels of genomicinstability (Bell et al. 2011).Embryonic fibroblasts from Atad5+/m mice exhibitmolecular defects in PCNA deubiquitination in response to DNA damage, as well asDNA damage hypersensitivity, high levels of genomic instability and aneuploidy.More than 90% of haploinsufficient Atad5+/m micedeveloped tumours such as sarcomas, carcinomas and adenocarcinomas thatexhibited high levels of genomic instability (Bell et al. 2011). This evidence concerns the gene ATAD5 and sarcoma.