Although aneuploid animals with reduced levels of BUB1, BUBR1, BUB3, RAE1, or both RAE1 and NUP98 fail to display an increase in spontaneous tumorigenesis, these mice are prone to carcinogen-induced tumors (69, 71–73), suggesting that aneuploidy does not initiate cancer in these mouse models, but rather drives tumor formation in cases in which mutations at oncogenic or tumor-suppressor loci have already increased the potential for cellular transformation. This evidence concerns the gene BUB1 and neoplasm.