Secondly, we only propose possible pathogenic pathways, and further experimental verification is needed, for example, we could test the effects of an artificial knockdown of MCM10 expression on tumor size and progression in cell models, validate qPCR results from tumor samples with Western blots, test for differences between MCM10 expression in CD8 mutant backgrounds and check if MCM10 expression differences cause differences in replication timing, genome stability or cell cycle defects. The gene discussed is MCM10; the disease is neoplasm.