Additionally, interactions between different genomic abnormalities, such as co-mutation patterns or multi-hit TP53 mutations, may account for some of the disease risk attributed to ontogeny in the McCarter paper; for example, one recent study found that two or more (rather than at least one) secondary-type mutation better defined a high-risk AML cohort [14]. This evidence concerns the gene TP53 and acute myeloid leukemia.