FAM50A and neoplasm: Further, we showed that co-disruption of FAM50A and FAM50B both in vitro and in vivo precipitates a profound reduction in tumour cell fitness, a phenotype that could be partially rescued by reintroduction of FAM50B. Importantly, we observed dysregulation of a range of cell regulatory transcriptional programmes and the formation of extensive micronuclei together with apoptotic cell death, suggesting a specific role for FAM50A/FAM50B in cellular survival via maintenance of genome stability.